Strain Name:

B6.129P2-Nos3tm1Unc/J

Stock Number:

002684

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Availability:

Level 4

Mice homozygous for the Nos3tm1Unc targeted mutation have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a challenging breeder.
Specieslaboratory mouse
Background Strain C57BL/6J
Donor Strain 129P2 via E14TG2a ES cell line
GenerationN12F36 (06-AUG-14)
Generation Definitions
 
Donating InvestigatorDr. Oliver Smithies,   University of North Carolina

Appearance
black
Related Genotype: a/a

Description
Mice homozygous for the Nos3tm1Unc targeted mutation are viable and fertile. They have elevated blood pressure that is about 20 mmHg higher than that seen in normal wildtype siblings. They also show a decreased heart rate. Female homozygotes are smaller in body weight than normal wildtype siblings. Hyperglycemic-euglycemic clamp studies demonstrate that homozygotes exhibit insulin resistance at the level of the liver and peripheral tissues.

Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to replace 129 bp of exon 12, which disrupted the calmodulin binding domain. The construct was electroporated into 129P2/OlaHsd-derived E14TG2a embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6J blastocysts and the resulting chimeric males were crossed to C57BL/6 female mice. Heterozygotes were intercrossed to generate homozygotes. The mice were subsequently backcrossed onto the C57BL/6J background for 12 generations.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls

Related Strains

Strains carrying   Nos3tm1Unc allele
008286   129S6.129P2(B6)-Nos3tm1Unc/J
018295   BKS.129P2(Cg)-Nos3tm1Unc/J
008340   BKS.Cg-Leprdb Nos3tm1Unc/RhrsJ
007073   CByJ.129P2(B6)-Nos3tm1Unc/J
022760   MRL.Cg-Nos3tm1Unc Faslpr/J
View Strains carrying   Nos3tm1Unc     (5 strains)

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms provided by MGI
- Model with phenotypic similarity to human disease where etiologies involve orthologs. Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
Hypertension, Essential
- Model with phenotypic similarity to human disease where etiologies are distinct. Human genes are associated with this disease. Orthologs of these genes do not appear in the mouse genotype(s).
Alveolar Capillary Dysplasia with Misalignment of Pulmonary Veins;
- Potential model based on gene homology relationships. Phenotypic similarity to the human disease has not been tested.
Alzheimer Disease; AD   (NOS3)
Nitric Oxide Synthase 3; NOS3   (NOS3)
Preeclampsia/Eclampsia 1; PEE1   (NOS3)
Stroke, Ischemic   (NOS3)
View Mammalian Phenotype Terms

Mammalian Phenotype Terms provided by MGI
      assigned by genotype

Nos3tm1Unc/Nos3+

        B6.129P2-Nos3tm1Unc/J
  • mortality/aging
  • partial postnatal lethality
    • 38% of mice die by P10 compared with 13% of wild-type mice   (MGI Ref ID J:103270)

Nos3tm1Unc/Nos3tm1Unc

        B6.129P2-Nos3tm1Unc/J
  • mortality/aging
  • partial neonatal lethality
    • about 40% die within the first hour of birth   (MGI Ref ID J:98913)
  • partial postnatal lethality
    • 85% of mice die by P10 compared with 13% of wild-type mice   (MGI Ref ID J:103270)
  • growth/size/body phenotype
  • fetal growth retardation
    • fetuses from E18 to term demonstrate slight growth retardation   (MGI Ref ID J:98913)
    • Intrauterine Growth Retardation demonstrated by ultrasonographic imaging showing differences in embryo and gestational vesicle measurements in both longitudinal and transversal curves from Days 5.5 to 14.5.   (MGI Ref ID J:140819)
  • cardiovascular system phenotype
  • abnormal angiogenesis
    • impaired pulmonary angiogenesis   (MGI Ref ID J:98913)
    • occasionally exhibit misalignment of pulmonary veins, which are seen in anomalous locations adjacent to the lung pleura, running alongside arterial vessels and sharing a common adventitial sheath   (MGI Ref ID J:98913)
    • abnormal vascular branching morphogenesis
      • E19.5 lungs show dramatic decrease of arteriolar branches and regions of marked capillary hypoperfusion   (MGI Ref ID J:98913)
  • abnormal glomerular capillary endothelium morphology
    • after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • abnormal heart morphology
    • diastolic dimension is increased compared to in wild-type mice   (MGI Ref ID J:103270)
    • abnormal interventricular septum membranous part morphology   (MGI Ref ID J:103270)
    • bicuspid aortic valve
      • high incidence (5 of 12) bicuspid aortic valves, however do not exhibit aortic coarctation   (MGI Ref ID J:103340)
    • enlarged heart atrium   (MGI Ref ID J:103270)
    • enlarged heart   (MGI Ref ID J:103270)
      • cardiac hypertrophy
        • in response to transverse aortic constriction (TAC)-induced pressure overload, wild-type hearts exhibit a progressive cardiac hypertrophy with significant dilatory remodeling whereas mutant hearts show more modest and concentric cardiac hypertrophy at 3 weeks, with minimal further progression   (MGI Ref ID J:98094)
        • at 9 weeks after TAC, mutant hearts develop significantly less intestitial fibrosis, myocyte hypertrophy, and fetal gene re-expression (B-natriuretic peptide and alpha-skeletal actin) relative wild-type hearts   (MGI Ref ID J:98094)
        • however, homozygotes show no significant differences in baseline heart weight or myocyte size relative to wild-type mice   (MGI Ref ID J:98094)
    • increased heart ventricle size
      • ventricular hypertrophy   (MGI Ref ID J:103270)
      • increased heart left ventricle size   (MGI Ref ID J:103270)
      • increased heart right ventricle size   (MGI Ref ID J:103270)
    • ostium secundum atrial septal defect   (MGI Ref ID J:103270)
    • ventricular septal defect
      • membranous and muscular ventricular defects in 6 of 10 mice compared with 1 of 10 atrial septal defects in wild-type mice   (MGI Ref ID J:103270)
      • muscular ventricular septal defect   (MGI Ref ID J:103270)
  • abnormal lung vasculature morphology
    • abnormalities in pulmonary vascular development   (MGI Ref ID J:98913)
    • disorganization of the extracellular matrix structure in the lung vasculature   (MGI Ref ID J:98913)
    • capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces   (MGI Ref ID J:98913)
    • pulmonary vascular congestion
      • severe with focal alveolar edema   (MGI Ref ID J:103270)
  • abnormal systemic arterial blood pressure
    • at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes fail to exhibit a further increase in systolic blood pressure relative to sham-operated homozygotes, unlike wild-type controls   (MGI Ref ID J:148626)
  • decreased cardiac muscle contractility   (MGI Ref ID J:103270)
  • decreased vascular endothelial cell number
    • after remnant kidney surgery, homozygotes exhibit a significantly greater decrease (50%) in endothelial cell density in the glomeruli and renal cortex relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • glomerular capillary thrombosis
    • after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • increased fetal cardiomyocyte apoptosis
    • in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium   (MGI Ref ID J:103270)
    • at E12.5, E15.5 and P1 in the myocardium   (MGI Ref ID J:103270)
  • increased left ventricle systolic pressure
    • in response to TAC-induced pressure overload, homozygotes exhibit a similar or greater rise in LV systolic pressure and ventricular afterload (arterial elastance [Ea]) at 9 weeks relative to wild-type mice   (MGI Ref ID J:98094)
  • increased ventricle muscle contractility
    • at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function   (MGI Ref ID J:98094)
  • kidney microaneurysm
    • after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • lung hemorrhage
    • E16 lungs show scattered areas of parenchymal and interlobar hemorrhages   (MGI Ref ID J:98913)
  • respiratory system phenotype
  • abnormal lung morphology
    • fetal lungs demonstrate abnormally compact lung structure and lungs of pups show evidence of septal thickening and reduced airspaces   (MGI Ref ID J:98913)
    • E20 lungs display absence of discernible basement membrane in the distal airways   (MGI Ref ID J:98913)
    • exhibit a decrease in apoptosis in the lungs   (MGI Ref ID J:98913)
    • E16 lungs display scattered subpleural hematomas   (MGI Ref ID J:98913)
    • abnormal lung vasculature morphology
      • abnormalities in pulmonary vascular development   (MGI Ref ID J:98913)
      • disorganization of the extracellular matrix structure in the lung vasculature   (MGI Ref ID J:98913)
      • capillaries of preterm mice remain deep within thickened septae, instead of aligning with the saccular epithelium, resulting in significantly fewer capillaries abutting saccular airspaces   (MGI Ref ID J:98913)
      • pulmonary vascular congestion
        • severe with focal alveolar edema   (MGI Ref ID J:103270)
    • abnormal type II pneumocyte morphology
      • observe an increase in markedly swollen glycogen laden pneumocytes protruding into airspaces compared to wild-type   (MGI Ref ID J:98913)
      • absent alveolar lamellar bodies
        • no evidence of lamellar bodies in type II pneumocytes   (MGI Ref ID J:98913)
    • thick pulmonary interalveolar septum
      • pups exhibit marked septal thickening   (MGI Ref ID J:98913)
  • abnormal surfactant secretion
    • lack of surfactant in bronchial alveolar lavage fluid   (MGI Ref ID J:103340)
  • lung hemorrhage
    • E16 lungs show scattered areas of parenchymal and interlobar hemorrhages   (MGI Ref ID J:98913)
  • pulmonary alveolar edema   (MGI Ref ID J:103270)
  • respiratory distress
    • some newborns exhibit severe respiratory distress   (MGI Ref ID J:98913)
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level
    • serum osteocalcin (BGLAP) levels are significantly higher in sham treated compared to wild-type sham mice at baseline, 14 weeks and remained higher   (MGI Ref ID J:129477)
    • serum TRAP5b (ACP5) concentrations are significantly higher in sham treated compared wild-type sham treated mice at all time points   (MGI Ref ID J:129477)
    • increased circulating creatine kinase level
      • after remnant kidney surgery, homozygotes exhibit a significantly higher increase in serum creatinine levels relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • albuminuria
    • after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • cyanosis
    • some newborns show varying levels of cyanosis   (MGI Ref ID J:98913)
  • glomerular capillary thrombosis
    • after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • increased blood urea nitrogen level
    • after remnant kidney surgery, homozygotes exhibit a significantly higher increase in BUN levels relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • pulmonary alveolar edema   (MGI Ref ID J:103270)
  • muscle phenotype
  • decreased cardiac muscle contractility   (MGI Ref ID J:103270)
  • increased ventricle muscle contractility
    • at 9 weeks of TAC, wild-type hearts exhibit a rightward shift of LV pressure-volume (PV) loops and end-systolic and end-diastolic PV relations reflecting remodeling; in contrast, mutant hearts display a leftward shift with smaller end-diastolic and end-systolic chamber volumes, as well as preserved wall thickness and fractional shortening, indicating preserved or enhanced systolic and diastolic function   (MGI Ref ID J:98094)
  • cellular phenotype
  • abnormal redox activity
    • in response to TAC-induced pressure overload, homozygotes (but not wild-type mice) exhibit blunted myocardial ROS generation and blunted nitrotyrosine, and gelatinase zymogen activity with no significant decline in the GSH/GSSH or NADPH/NADP ratio   (MGI Ref ID J:98094)
  • decreased kidney cell proliferation
    • after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • increased fetal cardiomyocyte apoptosis
    • in fetal atrioventricular endothelial cushions, septum primum and right and left ventricular myocardium   (MGI Ref ID J:103270)
    • at E12.5, E15.5 and P1 in the myocardium   (MGI Ref ID J:103270)
  • increased kidney apoptosis
    • at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • increased renal tubule apoptosis
      • in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance   (MGI Ref ID J:117046)
  • endocrine/exocrine gland phenotype
  • abnormal ovary morphology
    • on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls   (MGI Ref ID J:145649)
    • decreased corpora lutea number
      • on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively)   (MGI Ref ID J:145649)
    • small ovary
      • on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type   (MGI Ref ID J:145649)
  • reproductive system phenotype
  • abnormal ovary morphology
    • on day 0.5 of estrous cycle, mutant ovaries display a scarce number of ovulation sites and a higher number of anovulatory and luteinized unruptured follicles relative to wild-type controls   (MGI Ref ID J:145649)
    • decreased corpora lutea number
      • on day 0.5 of estrous cycle, mutant ovaries exhibit significantly less corpora lutea than wild-type ovaries (9.7 +/- 1.2 versus 14.2 +/- 1.2, respectively)   (MGI Ref ID J:145649)
    • small ovary
      • on day 0.5 of estrous cycle, mutant ovaries are significantly smaller than wild-type   (MGI Ref ID J:145649)
  • abnormal pregnancy
    • mutant dams show a higher incidence of embryo losses than wild-type dams (62.5% versus 16.7%, respectively)   (MGI Ref ID J:145649)
    • the mean rate of embryo losses detected in mutant dams is 49.90.1% versus less than 20% in wild-type dams   (MGI Ref ID J:145649)
    • in mutant dams, the highest %s of embryo losses occur between days 8.5 and 10.5 (55.6%) and at day 13.5 postcoitum (44.4% of total losses), whereas in control dams embryo losses occur at days 10.5 and 11.5 postcoitum   (MGI Ref ID J:145649)
    • impaired embryo implantation
      • on days 6.5 and 8.5 of pregnancy, the average number of embryos reaching implantation is lower in mutant mice relative to wild-type mice (4.0 +/- 0.4 versus 7.5 +/- 0.4, respectively)   (MGI Ref ID J:145649)
  • anovulation
    • female homozygotes display a higher rate of anovulation than wild-type controls (48.3 +/- 7.3% versus 29.7 +/- 6.3, respectively)   (MGI Ref ID J:145649)
  • decreased fertilization frequency
    • on day 0.5 of estrous cycle, female homozygotes show a significant reduction in the total number of recovered embryos (oocytes/zygotes) relative to wild-type controls (4.0 +/- 1.1 versus 10.4 +/- 1.6, respectively)   (MGI Ref ID J:145649)
    • thereafter, a mean of 2.0 +/- 1.0 of these recovered embryos are found to be fertilized, representing a non-fertilization rate of 50.7% versus only 3.3% in control littermates   (MGI Ref ID J:145649)
  • decreased ovulation rate
    • female homozygotes display a lower ovulation rate than wild-type controls (9.7 +/- 1.2% versus 14.2 +/- 1.2%, respectively)   (MGI Ref ID J:145649)
  • immune system phenotype
  • abnormal osteoclast physiology
    • serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points   (MGI Ref ID J:129477)
  • increased inflammatory response
    • fever in response to turpentine injection is enhanced compared to wild-type controls   (MGI Ref ID J:103018)
    • unlike in mice null for either Nos1 or Nos2, fever in response to LPS injection is not significantly different from wild-type controls   (MGI Ref ID J:103018)
    • kidney inflammation
      • after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
      • however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups   (MGI Ref ID J:148626)
  • renal/urinary system phenotype
  • abnormal kidney morphology
    • in 80% of adult freshly isolated kidneys indentations are observed, indicating zones of parenchymal scarring   (MGI Ref ID J:117046)
    • 4% of glomeruli outside scarred area exhibit loss of cellularity and vasculature, a hyalinization like appearance   (MGI Ref ID J:117046)
    • abnormal kidney cortex morphology
      • after remnant kidney surgery, homozygotes exhibit a 44% increase in tubulointerstitial injury relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
      • abnormal renal glomerulus morphology
        • glomeruli within scarred areas are considerably smaller than wild-type   (MGI Ref ID J:117046)
        • abnormal glomerular capillary endothelium morphology
          • after remnant kidney surgery, homozygotes exhibit a significantly greater endothelial cell loss than similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • expanded mesangial matrix
          • after remnant kidney surgery, homozygotes exhibit increased matrix deposition in some glomeruli unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • glomerular capillary thrombosis
          • after remnant kidney surgery, homozygotes develop intraluminal thrombi unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • glomerulosclerosis
          • within scarred areas   (MGI Ref ID J:117046)
          • after remnant kidney surgery, homozygotes develop significant glomerulosclerosis, unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • mesangial cell hyperplasia
          • after remnant kidney surgery, homozygotes exhibit increased mesangial proliferation relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • mesangiolysis
          • after remnant kidney surgery, homozygotes develop mesangiolysis unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • renal glomerulus fibrosis
          • after remnant kidney surgery, homozygotes exhibit a 46% increase in glomerular collagen IV deposition relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • renal glomerulus hypertrophy
          • after remnant kidney surgery, homozygotes develop significantly greater glomerular hypertrophy than similarly-treated wild-type controls   (MGI Ref ID J:148626)
        • renal glomerulus lipidosis
          • frequently a large lipid droplet is observed with Bowman's capsule and the adjacent matrix   (MGI Ref ID J:117046)
      • dilated renal glomerular capsule   (MGI Ref ID J:117046)
    • abnormal proximal convoluted tubule morphology
      • the glomeruli often display no clear connection to typical large-diameter proximal tubules   (MGI Ref ID J:117046)
    • abnormal renal tubule epithelium morphology
      • after remnant kidney surgery, homozygotes exhibit more severe sloughing , vacuolization and nuclear exfoliation of tubular epithelial cells relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • dilated renal tubules
      • after remnant kidney surgery, homozygotes exhibit more severe tubular dilatation than similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • kidney degeneration
      • degeneration of the glomerular core components is common within the scarred zones   (MGI Ref ID J:117046)
      • renal tubular necrosis
        • in 2 week old mice, as pyknotic nuclei and vacuolated cytoplasm are observed   (MGI Ref ID J:117046)
    • kidney microaneurysm
      • after remnant kidney surgery, homozygotes develop microaneurysms unlike similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • renal cast
      • after remnant kidney surgery, homozygotes exhibit more severe tubular cast formation than similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • renal hypoplasia
      • within scarred areas   (MGI Ref ID J:117046)
    • renal interstitial fibrosis
      • thin strands of connective tissue distributed loosely within the interglomerular interstitium   (MGI Ref ID J:117046)
      • after remnant kidney surgery, homozygotes exhibit a 38% increase in collagen III deposition in the tubulointerstitium relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • albuminuria
    • after remnant kidney surgery, homozygotes exhibit a significantly higher increase in urinary albumin excretion relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • decreased kidney cell proliferation
    • after remnant kidney surgery, homozygotes exhibit a 36% reduction of proliferating endothelial cells in cortical peritubular capillaries relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • increased kidney apoptosis
    • at 2 months after right subcapsular nephrectomy and surgical resection of the poles of the left kidney to produce a remnant kidney (RK) model, homozygotes exhibit a 4.6-fold increase in peritubular endothelial cell apoptosis relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • increased renal tubule apoptosis
      • in two week old mice based upon TUNEL staining and the presence of Apoptotic nuclei with a dense punctate appearance   (MGI Ref ID J:117046)
  • kidney failure
    • after remnant kidney surgery, homozygotes exhibit significantly worse renal function relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
  • kidney inflammation
    • after remnant kidney surgery, homozygotes exhibit increased macrophage infiltration in the glomeruli (15.4-fold) and in the tubulointerstitium (2.7-fold) relative to similarly-treated wild-type controls   (MGI Ref ID J:148626)
    • however, a similar increase in glomerular T-cell infiltration (62%) is seen in both RK groups   (MGI Ref ID J:148626)
  • skeleton phenotype
  • abnormal osteoblast physiology
    • serum osteocalcin (BGLAP) levels are significantly higher in sham compared wit wild-type sham mice at baseline and at 14 wk and remained higher   (MGI Ref ID J:129477)
  • abnormal osteoclast physiology
    • serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points   (MGI Ref ID J:129477)
  • decreased bone mineral density
    • exagerated BMD decrease in ovariectomized mice   (MGI Ref ID J:129477)
  • increased bone mineral density
    • between 10-20 weeks post sham-operation compared to sham-operated wild-type   (MGI Ref ID J:129477)
  • increased compact bone thickness
    • significantly greater cortical thickness in sham operated mice compared to sham operated wild-type mice   (MGI Ref ID J:129477)
  • hematopoietic system phenotype
  • abnormal osteoclast physiology
    • serum concentrations of TRAP5b (ACP5) are significantly higher in sham treated compared to wild-type sham treated mice at all time points   (MGI Ref ID J:129477)

Nos3tm1Unc/Nos3tm1Unc

        B6.129P2-Nos3tm1Unc
  • cardiovascular system phenotype
  • abnormal blood-brain barrier function
    • kainic acid injection of hippocampi does not cause blood-brain barrier breakdown   (MGI Ref ID J:150557)
  • nervous system phenotype
  • abnormal blood-brain barrier function
    • kainic acid injection of hippocampi does not cause blood-brain barrier breakdown   (MGI Ref ID J:150557)

The following phenotype information is associated with a similar, but not exact match to this JAX® Mice strain.

Nos3tm1Unc/Nos3+

        involves: 129P2/OlaHsd * C57BL/6J
  • cardiovascular system phenotype
  • increased vasodilation
    • aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187   (MGI Ref ID J:54772)
    • however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type   (MGI Ref ID J:54772)
  • muscle phenotype
  • increased vasodilation
    • aortic rings isolated from normotensive heterozygous mutant mice show normal endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187   (MGI Ref ID J:54772)
    • however, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are modestly enhanced in heterozygous aortic rings relative to wild-type   (MGI Ref ID J:54772)

Nos3tm1Unc/Nos3tm1Unc

        involves: 129P2/OlaHsd * C57BL/6
  • mortality/aging
  • decreased sensitivity to induced morbidity/mortality
    • after injection of platelet-activating factor (PAF), less than 10% mortality occurs within 30 minutes   (MGI Ref ID J:113106)
    • pretreatment with wortmannin before PAF treatment confers 100% protection to mutants and wild type pretreatment with wortmannin before PAF treatment confers 100% protection to mutants and wild-type   (MGI Ref ID J:113106)
    • in BSA-induced anaphylaxis, all mutants survive compared to fatality in 82% of controls; in OVA model, 92% of control mice die but all mutants survive challenge   (MGI Ref ID J:113106)
  • growth/size/body phenotype
  • decreased body weight
    • body weights at 14 weeks of age are approximately 7.5% lower than in wild-type   (MGI Ref ID J:36559)
    • body weight is signifcantly lower than controls at 14 days of age   (MGI Ref ID J:101254)
  • homeostasis/metabolism phenotype
  • decreased body temperature
    • challenge with BSA 2 weeks after sensitization with BSA induces severe hypothermia and mice succumb to systemic shock reaction; mutants show no mortality and only a delayed, mild, transient hypothermia   (MGI Ref ID J:113106)
    • similar results are seen with OVA-induced anaphylaxis   (MGI Ref ID J:113106)
  • increased circulating renin level
    • plasma renin concentrations are nearly twice as high as in wild-type   (MGI Ref ID J:36559)
  • cardiovascular system phenotype
  • abnormal cardiovascular system morphology   (MGI Ref ID J:101254)
    • abnormal heart weight
      • right ventricle/body weight ratio increased in males   (MGI Ref ID J:101254)
      • right ventricle/left ventricle+septum ratio increased in males   (MGI Ref ID J:101254)
    • abnormal pulmonary artery morphology
      • larger than in controls but only at 14 day   (MGI Ref ID J:101254)
      • medial wall area is greater than in controls in the fetus   (MGI Ref ID J:101254)
      • muscularity decreases after birth   (MGI Ref ID J:101254)
      • muscularity is reduced in the male but still greater than controls   (MGI Ref ID J:101254)
      • muscularity in females is like controls by 14 days of age   (MGI Ref ID J:101254)
  • abnormal cardiovascular system physiology   (MGI Ref ID J:101254)
    • abnormal heart right ventricle pressure
      • mean right ventricular pressure is elevated in males but not in females   (MGI Ref ID J:101254)
    • decreased heart rate
      • 670 beats per min vs. 709 beats per min in wild-type   (MGI Ref ID J:36559)
    • decreased vascular permeability
      • in BSA/BSA model of anaphylaxis, vascular permeability increased significantly in wild-type but very little in mutants; vascular leakage (extravasation) of Evans Blue dye (EB) is 2-fold lower than in wild-type mice   (MGI Ref ID J:113106)
      • in OVA/OVA model, no vascular permeability increase occurs in mutants and extravasation is significantly lower than in wild-type   (MGI Ref ID J:113106)
    • increased systemic arterial blood pressure   (MGI Ref ID J:36559)
      • increased mean systemic arterial blood pressure
        • elevated in males but not in females   (MGI Ref ID J:101254)
  • immune system phenotype
  • *normal* immune system phenotype
    • exhibit a similar susceptibility to lipopolysaccharide-induced death as wild type exhibit a similar susceptibility to lipopolysaccharide-induced death as wild-type   (MGI Ref ID J:36559)

Nos3tm1Unc/Nos3tm1Unc

        involves: 129P2/OlaHsd
  • mortality/aging
  • premature death
    • 50% of males die by 21 months of age, however female survival is similar to wild-type   (MGI Ref ID J:102136)
  • growth/size/body phenotype
  • decreased body weight
    • both males and females weight less than wild-type at 21 months of age   (MGI Ref ID J:102136)
  • cardiovascular system phenotype
  • abnormal heart morphology
    • at 21 months of age, males exhibit wall thinning of the heart while females display an increase in wall thickness of the heart   (MGI Ref ID J:102136)
    • abnormal interventricular septum morphology
      • females, but not males, exhibit a significant increase in diastolic septal wall thickness and to a lesser degree in the posterior wall   (MGI Ref ID J:102136)
      • males exhibit a decrease in interventricular septum thickening at 21 months of age   (MGI Ref ID J:102136)
    • cardiac hypertrophy
      • at 21 months of age, males have a large increase and females have a slight increase in heart size   (MGI Ref ID J:102136)
    • dilated heart left ventricle
      • left-ventricular end-systolic chamber dilation (LVESD) is increased about 45% in homozygous males compared to 25% in wild-type males at 21 months of age; no differences seen in females   (MGI Ref ID J:102136)
      • left ventricular mass (LVMASS) is increased in both males and females at 21 months of age   (MGI Ref ID J:102136)
      • ratio between LVMASS and LV volume is increased in 21 month old males   (MGI Ref ID J:102136)
    • increased heart weight
      • large increase in heart weight and heart weight to body weight ratio in males at 21 months of age and a smaller increase in females   (MGI Ref ID J:102136)
    • thin ventricular wall
      • males at 21 months of age, but not at 5.5 months, exhibit a decrease in left ventricular posterior wall   (MGI Ref ID J:102136)
  • abnormal systemic arterial blood pressure   (MGI Ref ID J:102136)
    • increased systemic arterial blood pressure
      • mean blood pressure is significantly elevated in both males and females at 5.5 months of age   (MGI Ref ID J:102136)
      • at 21 months of age, females, but not males, continue to exhibit increased mean blood pressure   (MGI Ref ID J:102136)
      • hypertension
        • arterial hypertension   (MGI Ref ID J:103153)
        • females are hypertensive at 7 months of age and maintain the elevated pressure at 21 months of age, however do not exhibit any contractile dysfunction   (MGI Ref ID J:102136)
      • increased systemic arterial diastolic blood pressure
        • elevated at 5.5 months of age in both males and females   (MGI Ref ID J:102136)
        • at 21 months of age, females, but not males, continue to exhibit an increased diastolic blood pressure   (MGI Ref ID J:102136)
      • increased systemic arterial systolic blood pressure
        • elevated at 5.5 months of age in both males and females   (MGI Ref ID J:102136)
        • at 21 months of age, females, but not males, continue to exhibit an increased systolic blood pressure   (MGI Ref ID J:102136)
  • decreased cardiac muscle contractility
    • males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age   (MGI Ref ID J:102136)
  • decreased vasodilation
    • insulin stimulation of muscle blood flow is about 40% smaller than in wild-type   (MGI Ref ID J:103153)
  • increased heart rate
    • heart rate is increased in males at 5.5 months of age but not at 21 months of age   (MGI Ref ID J:102136)
    • heart rate is normal in females at 5.5 months of age but remains elevated at 21 months of age and does not fall with age as in wild-type   (MGI Ref ID J:102136)
  • homeostasis/metabolism phenotype
  • abnormal blood homeostasis
    • plasma nitrite and nitrate concentrations are about 60% lower than in wild-type, indicating a defect of vascular NO production   (MGI Ref ID J:103153)
    • hyperlipidemia   (MGI Ref ID J:103153)
    • increased circulating cholesterol level
      • insulin-resistant homozygotes have 50% higher plasma levels of cholesterol   (MGI Ref ID J:103153)
    • increased circulating free fatty acid level
      • insulin-resistant homozygotes have a 2-fold elevation of free fatty acid   (MGI Ref ID J:103153)
    • increased circulating insulin level
      • fasting plasma insulin concentration is elevated almost 2-fold   (MGI Ref ID J:103153)
    • increased circulating triglyceride level
      • insulin-resistant homozygotes have a 2-fold elevation of triglycerides   (MGI Ref ID J:103153)
  • abnormal glucose homeostasis
    • glucose infusion rate, glucose turnover rate, and glucose clearance rate are 30-40% lower during a hyperinsulinemic euglycemic clamp study   (MGI Ref ID J:103153)
    • basal and insulin-stimulated glucose transport in isolated skeletal muscle is about 40% lower than in wild-type   (MGI Ref ID J:103153)
    • increased circulating insulin level
      • fasting plasma insulin concentration is elevated almost 2-fold   (MGI Ref ID J:103153)
    • insulin resistance
      • fasting hyperinsulinemia and glucose infusion rates during euglycemic clamp studies are 40% lower than in wild-type   (MGI Ref ID J:103153)
  • muscle phenotype
  • decreased cardiac muscle contractility
    • males, but not females, exhibit a marked decrease in ejection fraction and shortening fraction at 21 months of age   (MGI Ref ID J:102136)
  • decreased vasodilation
    • insulin stimulation of muscle blood flow is about 40% smaller than in wild-type   (MGI Ref ID J:103153)

Nos3tm1Unc/Nos3tm1Unc

        involves: 129P2/OlaHsd * C57BL/6J
  • cardiovascular system phenotype
  • abnormal vasodilation
    • aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187   (MGI Ref ID J:54772)
    • in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values   (MGI Ref ID J:54772)
  • decreased heart rate   (MGI Ref ID J:36559)
    • homozygotes display mild bradycardia relative to wild-type mice   (MGI Ref ID J:54772)
    • notably, chronic treatment of homozygotes with L-NAME induces a significant decrease of heart rate in both wild-type mice and mutant mice   (MGI Ref ID J:54772)
  • increased systemic arterial blood pressure
    • increase in blood pressure by about 18 mmHg   (MGI Ref ID J:36559)
    • hypertension
      • homozygotes exhibit modest hypertension relative to wild-type mice   (MGI Ref ID J:54772)
      • chronic treatment of homozygotes with NOS inhibitor L-NAME fails to further increase blood pressure; in contrast, chronic L-NAME treatment increases blood pressure in wild-type (C57BL/6J) mice to a level similar to that noted in mutant mice   (MGI Ref ID J:54772)
  • increased vasoconstriction
    • aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin   (MGI Ref ID J:54772)
  • growth/size/body phenotype
  • decreased body weight
    • body weight is approximately 7.5% lower than wild-type at 14 weeks of age   (MGI Ref ID J:36559)
  • homeostasis/metabolism phenotype
  • *normal* homeostasis/metabolism phenotype
    • unlike mice null for Nos1 or Nos2, no abnormalities in urine pH or bicarbonate concentrations are detected   (MGI Ref ID J:64896)
    • increased circulating renin level
      • plasma renin is nearly 2x that of wild-type   (MGI Ref ID J:36559)
  • muscle phenotype
  • abnormal vasodilation
    • aortic rings isolated from homozygous mutant mice show complete loss of endothelium-dependent vasorelaxation induced by acetylcholine and the calcium ionophore A23187   (MGI Ref ID J:54772)
    • in contrast, vasorelaxations to the endothelium-independent vasodilator nitroglycerin are enhanced resulting in a shift of EC50 by ~7-fold relative to wild-type values   (MGI Ref ID J:54772)
  • increased vasoconstriction
    • aortic rings isolated from homozygous mutant mice exhibit a significantly enhanced vasoconstriction in response to phenylephrine and a modestly enhanced vasoconstriction in response to serotonin   (MGI Ref ID J:54772)

Nos3tm1Unc/Nos3tm1Unc

        BKS.129P2-Nos3tm1Unc
  • renal/urinary system phenotype
  • albuminuria
    • moderate albuminuria is observed at 26 weeks of age   (MGI Ref ID J:135864)
  • homeostasis/metabolism phenotype
  • albuminuria
    • moderate albuminuria is observed at 26 weeks of age   (MGI Ref ID J:135864)
  • cardiovascular system phenotype
  • increased systemic arterial systolic blood pressure
    • observed by 24 to 28 weeks of age   (MGI Ref ID J:135864)
View Research Applications

Research Applications
This mouse can be used to support research in many areas including:

Internal/Organ Research
Wound Healing
      delayed/impaired

Nos3tm1Unc related

Cardiovascular Research
Heart Abnormalities
      bradycardia
Hypertension

Diabetes and Obesity Research
Insulin Resistance

Internal/Organ Research
Heart Abnormalities

Genes & Alleles

Gene & Allele Information provided by MGI

 
Allele Symbol Nos3tm1Unc
Allele Name targeted mutation 1, University of North Carolina
Allele Type Targeted (Null/Knockout)
Common Name(s) NOS3-; eNOS-; eNOSKO; ecNOS-;
Mutation Made ByDr. Oliver Smithies,   University of North Carolina
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Nos3, nitric oxide synthase 3, endothelial cell
Chromosome 5
Gene Common Name(s) 2310065A03Rik; ECNOS; Nos-3; RIKEN cDNA 2310065A03 gene; eNOS; nitric oxide synthase 3 (indicible);
General Note Phenotypic Similarity to Human Syndrome: Aortic Valve Disease in Homozygous mice (J:103340)
Molecular Note A 1.2 kb neomycin cassette replaced 129 bp of exon 12 of the gene. This disrupted the calmodulin binding site of the protein and introduced a premature stop codon into the transcripts. Immunohistochemisty of heart and kidney sections from homozygous mutant mice confirmed that no detectable encoded protein was present. [MGI Ref ID J:36559]

Genotyping

Genotyping Information

Genotyping Protocols

Nnt,

Separated MCA


Nos3tm1Unc, High Resolution Melting
Nos3tm1Unc, Standard PCR


Helpful Links

Genotyping resources and troubleshooting

References

References provided by MGI

Selected Reference(s)

Shesely EG; Maeda N; Kim HS; Desai KM; Krege JH; Laubach VE; Sherman PA; Sessa WC; Smithies O. 1996. Elevated blood pressures in mice lacking endothelial nitric oxide synthase. Proc Natl Acad Sci U S A 93(23):13176-81. [PubMed: 8917564]  [MGI Ref ID J:36559]

Additional References

Barouch LA; Harrison RW; Skaf MW; Rosas GO; Cappola TP; Kobeissi ZA; Hobai IA; Lemmon CA; Burnett AL; O'Rourke B; Rodriguez ER; Huang PL; Lima JA; Berkowitz DE; Hare JM. 2002. Nitric oxide regulates the heart by spatial confinement of nitric oxide synthase isoforms. Nature 416(6878):337-9. [PubMed: 11907582]  [MGI Ref ID J:75645]

Harada H; Pavlick KP; Hines IN; Lefer DJ; Hoffman JM; Bharwani S; Wolf RE; Grisham MB. 2003. Sexual dimorphism in reduced-size liver ischemia and reperfusion injury in mice: role of endothelial cell nitric oxide synthase. Proc Natl Acad Sci U S A 100(2):739-44. [PubMed: 12522262]  [MGI Ref ID J:81420]

Kaminski A; Pohl CB; Sponholz C; Ma N; Stamm C; Vollmar B; Steinhoff G. 2004. Up-regulation of endothelial nitric oxide synthase inhibits pulmonary leukocyte migration following lung ischemia-reperfusion in mice. Am J Pathol 164(6):2241-9. [PubMed: 15161656]  [MGI Ref ID J:91099]

Shankar RR; Wu Y; Shen HQ; Zhu JS; Baron AD. 2000. Mice with gene disruption of both endothelial and neuronal nitric oxide synthase exhibit insulin resistance. Diabetes 49(5):684-7. [PubMed: 10905473]  [MGI Ref ID J:62229]

Tranguch S; Huet-Hudson Y. 2003. Decreased viability of nitric oxide synthase double knockout mice. Mol Reprod Dev 65(2):175-9. [PubMed: 12704728]  [MGI Ref ID J:83112]

de Jonge WJ; Hallemeesch MM; Kwikkers KL; Ruijter JM; de Gier-de Vries C; van Roon MA; Meijer AJ; Marescau B; de Deyn PP; Deutz NE; Lamers WH. 2002. Overexpression of arginase I in enterocytes of transgenic mice elicits a selective arginine deficiency and affects skin, muscle, and lymphoid development. Am J Clin Nutr 76(1):128-40. [PubMed: 12081826]  [MGI Ref ID J:80556]

Nos3tm1Unc related

Abudukadier A; Fujita Y; Obara A; Ohashi A; Fukushima T; Sato Y; Ogura M; Nakamura Y; Fujimoto S; Hosokawa M; Hasegawa H; Inagaki N. 2013. Tetrahydrobiopterin has a glucose-lowering effect by suppressing hepatic gluconeogenesis in an endothelial nitric oxide synthase-dependent manner in diabetic mice. Diabetes 62(9):3033-43. [PubMed: 23649519]  [MGI Ref ID J:208962]

Addabbo F; Ratliff B; Park HC; Kuo MC; Ungvari Z; Ciszar A; Krasnikof B; Sodhi K; Zhang F; Nasjletti A; Goligorsky MS. 2009. The Krebs cycle and mitochondrial mass are early victims of endothelial dysfunction: proteomic approach. Am J Pathol 174(1):34-43. [PubMed: 19095954]  [MGI Ref ID J:144210]

Adler S; Huang H; Loke KE; Xu X; Tada H; Laumas A; Hintze TH. 2001. Endothelial nitric oxide synthase plays an essential role in regulation of renal oxygen consumption by NO. Am J Physiol Renal Physiol 280(5):F838-43. [PubMed: 11292626]  [MGI Ref ID J:69293]

Advani A; Huang Q; Thai K; Advani SL; White KE; Kelly DJ; Yuen DA; Connelly KA; Marsden PA; Gilbert RE. 2011. Long-Term Administration of the Histone Deacetylase Inhibitor Vorinostat Attenuates Renal Injury in Experimental Diabetes through an Endothelial Nitric Oxide Synthase-Dependent Mechanism. Am J Pathol 178(5):2205-14. [PubMed: 21514434]  [MGI Ref ID J:171586]

Ahmadie R; Santiago JJ; Walker J; Fang T; Le K; Zhao Z; Azordegan N; Bage S; Lytwyn M; Rattan S; Dixon IM; Kardami E; Moghadasian MH; Jassal DS. 2010. A high-lipid diet potentiates left ventricular dysfunction in nitric oxide synthase 3-deficient mice after chronic pressure overload. J Nutr 140(8):1438-44. [PubMed: 20554900]  [MGI Ref ID J:162084]

Akita Y; Otani H; Matsuhisa S; Kyoi S; Enoki C; Hattori R; Imamura H; Kamihata H; Kimura Y; Iwasaka T. 2007. Exercise-induced activation of cardiac sympathetic nerve triggers cardioprotection via redox-sensitive activation of eNOS and upregulation of iNOS. Am J Physiol Heart Circ Physiol 292(5):H2051-9. [PubMed: 17259438]  [MGI Ref ID J:125942]

Al Gadban MM; German J; Truman JP; Soodavar F; Riemer EC; Twal WO; Smith KJ; Heller D; Hofbauer AF; Oates JC; Hammad SM. 2012. Lack of nitric oxide synthases increases lipoprotein immune complex deposition in the aorta and elevates plasma sphingolipid levels in lupus. Cell Immunol 276(1-2):42-51. [PubMed: 22560558]  [MGI Ref ID J:188295]

Almodovar AJ; Luther RJ; Stonebrook CL; Wood PA. 2013. Genomic structure and genetic drift in C57BL/6 congenic metabolic mutant mice. Mol Genet Metab 110(3):396-400. [PubMed: 23867526]  [MGI Ref ID J:205314]

Arraj M; Lemmer B. 2006. Circadian rhythms in heart rate, motility, and body temperature of wild-type C57 and eNOS knock-out mice under light-dark, free-run, and after time zone transition. Chronobiol Int 23(4):795-812. [PubMed: 16887749]  [MGI Ref ID J:124720]

Austin SA; Santhanam AV; Hinton DJ; Choi DS; Katusic ZS. 2013. Endothelial nitric oxide deficiency promotes Alzheimer's disease pathology. J Neurochem :. [PubMed: 23745722]  [MGI Ref ID J:203972]

Austin SA; Santhanam AV; Katusic ZS. 2010. Endothelial nitric oxide modulates expression and processing of amyloid precursor protein. Circ Res 107(12):1498-502. [PubMed: 21127294]  [MGI Ref ID J:178507]

Balasubramaniam V; Maxey AM; Morgan DB; Markham NE; Abman SH. 2006. Inhaled NO restores lung structure in eNOS-deficient mice recovering from neonatal hypoxia. Am J Physiol Lung Cell Mol Physiol 291(1):L119-27. [PubMed: 16443642]  [MGI Ref ID J:121213]

Baumbach GL; Sigmund CD; Faraci FM. 2004. Structure of cerebral arterioles in mice deficient in expression of the gene for endothelial nitric oxide synthase. Circ Res 95(8):822-9. [PubMed: 15388643]  [MGI Ref ID J:102298]

Bearden SE. 2007. Advancing age produces sex differences in vasomotor kinetics during and after skeletal muscle contraction. Am J Physiol Regul Integr Comp Physiol 293(3):R1274-9. [PubMed: 17626125]  [MGI Ref ID J:124699]

Beierwaltes WH; Potter DL; Shesely EG. 2002. Renal baroreceptor-stimulated renin in the eNOS knockout mouse. Am J Physiol Renal Physiol 282(1):F59-64. [PubMed: 11739113]  [MGI Ref ID J:75596]

Bergula AP; Haidekker MA; Huang W; Stevens HY; Frangos JA. 2004. Venous ligation-mediated bone adaptation is NOS 3 dependent. Bone 34(3):562-9. [PubMed: 15003804]  [MGI Ref ID J:109405]

Bernatchez P; Sharma A; Bauer PM; Marin E; Sessa WC. 2011. A noninhibitory mutant of the caveolin-1 scaffolding domain enhances eNOS-derived NO synthesis and vasodilation in mice. J Clin Invest 121(9):3747-55. [PubMed: 21804187]  [MGI Ref ID J:178265]

Bhandari V; Choo-Wing R; Harijith A; Sun H; Syed MA; Homer RJ; Elias JA. 2012. Increased hyperoxia-induced lung injury in nitric oxide synthase 2 null mice is mediated via angiopoietin 2. Am J Respir Cell Mol Biol 46(5):668-76. [PubMed: 22227562]  [MGI Ref ID J:196034]

Borniquel S; Valle I; Cadenas S; Lamas S; Monsalve M. 2006. Nitric oxide regulates mitochondrial oxidative stress protection via the transcriptional coactivator PGC-1alpha. FASEB J 20(11):1889-91. [PubMed: 16891621]  [MGI Ref ID J:112736]

Boyer L; Plantier L; Dagouassat M; Lanone S; Goven D; Caramelle P; Berrehar F; Kerbrat S; Dinh-Xuan AT; Crestani B; Le Gouvello S; Boczkowski J. 2011. Role of nitric oxide synthases in elastase-induced emphysema. Lab Invest 91(3):353-62. [PubMed: 20956973]  [MGI Ref ID J:169267]

Bucci M; Roviezzo F; Posadas I; Yu J; Parente L; Sessa WC; Ignarro LJ; Cirino G. 2005. Endothelial nitric oxide synthase activation is critical for vascular leakage during acute inflammation in vivo. Proc Natl Acad Sci U S A 102(3):904-8. [PubMed: 15640348]  [MGI Ref ID J:96126]

Budzyn K; Marley PD; Sobey CG. 2004. Chronic mevastatin modulates receptor-dependent vascular contraction in eNOS-deficient mice. Am J Physiol Regul Integr Comp Physiol 287(2):R342-8. [PubMed: 15130878]  [MGI Ref ID J:95774]

Buys ES; Raher MJ; Blake SL; Neilan TG; Graveline AR; Passeri JJ; Llano M; Perez-Sanz TM; Ichinose F; Janssens S; Zapol WM; Picard MH; Bloch KD; Scherrer-Crosbie M. 2007. Cardiomyocyte-restricted restoration of nitric oxide synthase 3 attenuates left ventricular remodeling after chronic pressure overload. Am J Physiol Heart Circ Physiol 293(1):H620-7. [PubMed: 17416602]  [MGI Ref ID J:126032]

Cabou C; Cani PD; Campistron G; Knauf C; Mathieu C; Sartori C; Amar J; Scherrer U; Burcelin R. 2007. Central insulin regulates heart rate and arterial blood flow: an endothelial nitric oxide synthase-dependent mechanism altered during diabetes. Diabetes 56(12):2872-7. [PubMed: 17804761]  [MGI Ref ID J:142487]

Cabrales P; Tsai AG; Frangos JA; Intaglietta M. 2005. Role of endothelial nitric oxide in microvascular oxygen delivery and consumption. Free Radic Biol Med 39(9):1229-37. [PubMed: 16214038]  [MGI Ref ID J:102115]

Calingasan NY; Huang PL; Chun HS; Fabian A; Gibson GE. 2000. Vascular factors are critical in selective neuronal loss in an animal model of impaired oxidative metabolism. J Neuropathol Exp Neurol 59(3):207-17. [PubMed: 10744059]  [MGI Ref ID J:62409]

Carlstrom M; Larsen FJ; Nystrom T; Hezel M; Borniquel S; Weitzberg E; Lundberg JO. 2010. Dietary inorganic nitrate reverses features of metabolic syndrome in endothelial nitric oxide synthase-deficient mice. Proc Natl Acad Sci U S A 107(41):17716-20. [PubMed: 20876122]  [MGI Ref ID J:165402]

Carraway MS; Suliman HB; Jones WS; Chen CW; Babiker A; Piantadosi CA. 2010. Erythropoietin activates mitochondrial biogenesis and couples red cell mass to mitochondrial mass in the heart. Circ Res 106(11):1722-30. [PubMed: 20395592]  [MGI Ref ID J:172704]

Castrop H; Schweda F; Mizel D; Huang Y; Briggs J; Kurtz A; Schnermann J. 2004. Permissive role of nitric oxide in macula densa control of renin secretion. Am J Physiol Renal Physiol 286(5):F848-57. [PubMed: 15075180]  [MGI Ref ID J:113763]

Cauwels A; Buys ES; Thoonen R; Geary L; Delanghe J; Shiva S; Brouckaert P. 2009. Nitrite protects against morbidity and mortality associated with TNF- or LPS-induced shock in a soluble guanylate cyclase-dependent manner. J Exp Med 206(13):2915-24. [PubMed: 19934018]  [MGI Ref ID J:155687]

Cauwels A; Janssen B; Buys E; Sips P; Brouckaert P. 2006. Anaphylactic shock depends on PI3K and eNOS-derived NO. J Clin Invest 116(8):2244-51. [PubMed: 16886062]  [MGI Ref ID J:113106]

Champion HC; Georgakopoulos D; Takimoto E; Isoda T; Wang Y; Kass DA. 2004. Modulation of in vivo cardiac function by myocyte-specific nitric oxide synthase-3. Circ Res 94(5):657-63. [PubMed: 14752030]  [MGI Ref ID J:97591]

Chang AC; Fu Y; Garside VC; Niessen K; Chang L; Fuller M; Setiadi A; Smrz J; Kyle A; Minchinton A; Marra M; Hoodless PA; Karsan A. 2011. Notch initiates the endothelial-to-mesenchymal transition in the atrioventricular canal through autocrine activation of soluble guanylyl cyclase. Dev Cell 21(2):288-300. [PubMed: 21839921]  [MGI Ref ID J:184890]

Chatterjee S; Lardinois O; Bonini MG; Bhattacharjee S; Stadler K; Corbett J; Deterding LJ; Tomer KB; Kadiiska M; Mason RP. 2009. Site-specific carboxypeptidase B1 tyrosine nitration and pathophysiological implications following its physical association with nitric oxide synthase-3 in experimental sepsis. J Immunol 183(6):4055-66. [PubMed: 19717511]  [MGI Ref ID J:152293]

Cheng AM; Rizzo-DeLeon N; Wilson CL; Lee WJ; Tateya S; Clowes AW; Schwartz MW; Kim F. 2014. Vasodilator-stimulated phosphoprotein protects against vascular inflammation and insulin resistance. Am J Physiol Endocrinol Metab 307(7):E571-9. [PubMed: 25117404]  [MGI Ref ID J:215575]

Cheng H; Fan X; Moeckel GW; Harris RC. 2011. Podocyte COX-2 exacerbates diabetic nephropathy by increasing podocyte (pro)renin receptor expression. J Am Soc Nephrol 22(7):1240-51. [PubMed: 21737546]  [MGI Ref ID J:179350]

Chiang E; Dang O; Anderson K; Matsuzawa A; Ichijo H; David M. 2006. Cutting edge: apoptosis-regulating signal kinase 1 is required for reactive oxygen species-mediated activation of IFN regulatory factor 3 by lipopolysaccharide. J Immunol 176(10):5720-4. [PubMed: 16670275]  [MGI Ref ID J:131688]

Chiossi G; Costantine MM; Tamayo EH; Orise P; Hankins GD; Saade GR; Longo M. 2011. Effect of age and gender on the progression of adult vascular dysfunction in a mouse model of fetal programming lacking endothelial nitric oxide synthase. Am J Physiol Heart Circ Physiol :. [PubMed: 21572009]  [MGI Ref ID J:173237]

Choi HC; Song P; Xie Z; Wu Y; Xu J; Zhang M; Dong Y; Wang S; Lau K; Zou MH. 2008. Reactive nitrogen species is required for the activation of the AMP-activated protein kinase by statin in vivo. J Biol Chem 283(29):20186-97. [PubMed: 18474592]  [MGI Ref ID J:138750]

Coletta C; Papapetropoulos A; Erdelyi K; Olah G; Modis K; Panopoulos P; Asimakopoulou A; Gero D; Sharina I; Martin E; Szabo C. 2012. Hydrogen sulfide and nitric oxide are mutually dependent in the regulation of angiogenesis and endothelium-dependent vasorelaxation. Proc Natl Acad Sci U S A 109(23):9161-6. [PubMed: 22570497]  [MGI Ref ID J:184767]

Connelly L; Madhani M; Hobbs AJ. 2005. Resistance to endotoxic shock in endothelial nitric-oxide synthase (eNOS) knock-out mice: a pro-inflammatory role for eNOS-derived no in vivo. J Biol Chem 280(11):10040-6. [PubMed: 15647265]  [MGI Ref ID J:97766]

Cook S; Hugli O; Egli M; Menard B; Thalmann S; Sartori C; Perrin C; Nicod P; Thorens B; Vollenweider P; Scherrer U; Burcelin R. 2004. Partial gene deletion of endothelial nitric oxide synthase predisposes to exaggerated high-fat diet-induced insulin resistance and arterial hypertension. Diabetes 53(8):2067-72. [PubMed: 15277387]  [MGI Ref ID J:107196]

Csiszar A; Labinskyy N; Pinto JT; Ballabh P; Zhang H; Losonczy G; Pearson K; de Cabo R; Pacher P; Zhang C; Ungvari Z. 2009. Resveratrol induces mitochondrial biogenesis in endothelial cells. Am J Physiol Heart Circ Physiol 297(1):H13-20. [PubMed: 19429820]  [MGI Ref ID J:151104]

Cui X; Chopp M; Zacharek A; Ning R; Ding X; Roberts C; Chen J. 2013. Endothelial nitric oxide synthase regulates white matter changes via the BDNF/TrkB pathway after stroke in mice. PLoS One 8(11):e80358. [PubMed: 24236179]  [MGI Ref ID J:209313]

Cui X; Chopp M; Zacharek A; Zhang C; Roberts C; Chen J. 2009. Role of endothelial nitric oxide synthetase in arteriogenesis after stroke in mice. Neuroscience 159(2):744-50. [PubMed: 19154781]  [MGI Ref ID J:148965]

Dachtler J; Hardingham NR; Glazewski S; Wright NF; Blain EJ; Fox K. 2011. Experience-Dependent Plasticity Acts via GluR1 and a Novel Neuronal Nitric Oxide Synthase-Dependent Synaptic Mechanism in Adult Cortex. J Neurosci 31(31):11220-30. [PubMed: 21813683]  [MGI Ref ID J:174589]

Dai X; Faber JE. 2010. Endothelial nitric oxide synthase deficiency causes collateral vessel rarefaction and impairs activation of a cell cycle gene network during arteriogenesis. Circ Res 106(12):1870-81. [PubMed: 20431061]  [MGI Ref ID J:175053]

Deeb RS; Shen H; Gamss C; Gavrilova T; Summers BD; Kraemer R; Hao G; Gross SS; Laine M; Maeda N; Hajjar DP; Upmacis RK. 2006. Inducible nitric oxide synthase mediates prostaglandin h2 synthase nitration and suppresses eicosanoid production. Am J Pathol 168(1):349-62. [PubMed: 16400036]  [MGI Ref ID J:104432]

Di Lorenzo A; Lin MI; Murata T; Landskroner-Eiger S; Schleicher M; Kothiya M; Iwakiri Y; Yu J; Huang PL; Sessa WC. 2013. eNOS-derived nitric oxide regulates endothelial barrier function through VE-cadherin and Rho GTPases. J Cell Sci 126(Pt 24):5541-52. [PubMed: 24046447]  [MGI Ref ID J:211218]

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Stanley JL; Andersson IJ; Hirt CJ; Moore L; Dilworth MR; Chade AR; Sibley CP; Davidge ST; Baker PN. 2012. Effect of the anti-oxidant tempol on fetal growth in a mouse model of fetal growth restriction. Biol Reprod 87(1):25, 1-8. [PubMed: 22423051]  [MGI Ref ID J:192382]

Steed MM; Tyagi N; Sen U; Schuschke DA; Joshua IG; Tyagi SC. 2010. Functional consequences of the collagen/elastin switch in vascular remodeling in hyperhomocysteinemic wild-type, eNOS-/-, and iNOS-/- mice. Am J Physiol Lung Cell Mol Physiol 299(3):L301-11. [PubMed: 20581102]  [MGI Ref ID J:164613]

Stobart JL; Lu L; Anderson HD; Mori H; Anderson CM. 2013. Astrocyte-induced cortical vasodilation is mediated by D-serine and endothelial nitric oxide synthase. Proc Natl Acad Sci U S A 110(8):3149-54. [PubMed: 23386721]  [MGI Ref ID J:194537]

Suliman HB; Carraway MS; Tatro LG; Piantadosi CA. 2007. A new activating role for CO in cardiac mitochondrial biogenesis. J Cell Sci 120(Pt 2):299-308. [PubMed: 17179207]  [MGI Ref ID J:117460]

Sun D; Cuevas AJ; Gotlinger K; Hwang SH; Hammock BD; Schwartzman ML; Huang A. 2014. Soluble epoxide hydrolase-dependent regulation of myogenic response and blood pressure. Am J Physiol Heart Circ Physiol 306(8):H1146-53. [PubMed: 24561863]  [MGI Ref ID J:210751]

Sun D; Huang A; Smith CJ; Stackpole CJ; Connetta JA; Shesely EG ; Koller A ; Kaley G. 1999. Enhanced release of prostaglandins contributes to flow-induced arteriolar dilation in eNOS knockout mice. Circ Res 85(3):288-93. [PubMed: 10436172]  [MGI Ref ID J:57415]

Sun D; Liu H; Yan C; Jacobson A; Ojaimi C; Huang A; Kaley G. 2006. COX-2 contributes to the maintenance of flow-induced dilation in arterioles of eNOS-knockout mice. Am J Physiol Heart Circ Physiol 291(3):H1429-35. [PubMed: 16632543]  [MGI Ref ID J:116431]

Sun D; Yang YM; Jiang H; Wu H; Ojaimi C; Kaley G; Huang A. 2010. Roles of CYP2C29 and RXR gamma in vascular EET synthesis of female mice. Am J Physiol Regul Integr Comp Physiol 298(4):R862-9. [PubMed: 20130225]  [MGI Ref ID J:158784]

Sun J; Picht E; Ginsburg KS; Bers DM; Steenbergen C; Murphy E. 2006. Hypercontractile female hearts exhibit increased S-nitrosylation of the L-type Ca2+ channel alpha1 subunit and reduced ischemia/reperfusion injury. Circ Res 98(3):403-11. [PubMed: 16397145]  [MGI Ref ID J:118890]

Sun YB; Qu X; Li X; Nikolic-Paterson DJ; Li J. 2013. Endothelial dysfunction exacerbates renal interstitial fibrosis through enhancing fibroblast Smad3 linker phosphorylation in the mouse obstructed kidney. PLoS One 8(12):e84063. [PubMed: 24391884]  [MGI Ref ID J:209832]

Sun YB; Qu X; Zhang X; Caruana G; Bertram JF; Li J. 2013. Glomerular endothelial cell injury and damage precedes that of podocytes in adriamycin-induced nephropathy. PLoS One 8(1):e55027. [PubMed: 23359116]  [MGI Ref ID J:195801]

Suzuki N; Motohashi N; Uezumi A; Fukada S; Yoshimura T; Itoyama Y; Aoki M; Miyagoe-Suzuki Y; Takeda S. 2007. NO production results in suspension-induced muscle atrophy through dislocation of neuronal NOS. J Clin Invest 117(9):2468-76. [PubMed: 17786240]  [MGI Ref ID J:127415]

Tada H; Thompson CI; Recchia FA; Loke KE; Ochoa M; Smith CJ; Shesely EG; Kaley G; Hintze TH. 2000. Myocardial glucose uptake is regulated by nitric oxide via endothelial nitric oxide synthase in Langendorff mouse heart. Circ Res 86(3):270-4. [PubMed: 10679477]  [MGI Ref ID J:110253]

Takimoto E; Champion HC; Belardi D; Moslehi J; Mongillo M; Mergia E; Montrose DC; Isoda T; Aufiero K; Zaccolo M; Dostmann WR; Smith CJ; Kass DA. 2005. cGMP catabolism by phosphodiesterase 5A regulates cardiac adrenergic stimulation by NOS3-dependent mechanism. Circ Res 96(1):100-9. [PubMed: 15576651]  [MGI Ref ID J:104469]

Takimoto E; Champion HC; Li M; Ren S; Rodriguez ER; Tavazzi B; Lazzarino G; Paolocci N; Gabrielson KL; Wang Y; Kass DA. 2005. Oxidant stress from nitric oxide synthase-3 uncoupling stimulates cardiac pathologic remodeling from chronic pressure load. J Clin Invest 115(5):1221-1231. [PubMed: 15841206]  [MGI Ref ID J:98094]

Talukder MA; Yang F; Shimokawa H; Zweier JL. 2010. eNOS is required for acute in vivo ischemic preconditioning of the heart: effects of ischemic duration and sex. Am J Physiol Heart Circ Physiol 299(2):H437-45. [PubMed: 20525875]  [MGI Ref ID J:163868]

Tanabe K; Lanaspa MA; Kitagawa W; Rivard CJ; Miyazaki M; Klawitter J; Schreiner GF; Saleem MA; Mathieson PW; Makino H; Johnson RJ; Nakagawa T. 2012. Nicorandil as a novel therapy for advanced diabetic nephropathy in the eNOS-deficient mouse. Am J Physiol Renal Physiol 302(9):F1151-60. [PubMed: 22338086]  [MGI Ref ID J:183413]

Tateya S; Rizzo NO; Handa P; Cheng AM; Morgan-Stevenson V; Daum G; Clowes AW; Morton GJ; Schwartz MW; Kim F. 2011. Endothelial NO/cGMP/VASP signaling attenuates Kupffer cell activation and hepatic insulin resistance induced by high-fat feeding. Diabetes 60(11):2792-801. [PubMed: 21911751]  [MGI Ref ID J:189496]

Tedesco L; Valerio A; Dossena M; Cardile A; Ragni M; Pagano C; Pagotto U; Carruba MO; Vettor R; Nisoli E. 2010. Cannabinoid receptor stimulation impairs mitochondrial biogenesis in mouse white adipose tissue, muscle, and liver: the role of eNOS, p38 MAPK, and AMPK pathways. Diabetes 59(11):2826-36. [PubMed: 20739683]  [MGI Ref ID J:169336]

Theodorakis NG; Wang YN; Skill NJ; Metz MA; Cahill PA; Redmond EM; Sitzmann JV. 2003. The role of nitric oxide synthase isoforms in extrahepatic portal hypertension: studies in gene-knockout mice. Gastroenterology 124(5):1500-8. [PubMed: 12730888]  [MGI Ref ID J:107756]

Thibeault S; Rautureau Y; Oubaha M; Faubert D; Wilkes BC; Delisle C; Gratton JP. 2010. S-nitrosylation of beta-catenin by eNOS-derived NO promotes VEGF-induced endothelial cell permeability. Mol Cell 39(3):468-76. [PubMed: 20705246]  [MGI Ref ID J:163677]

Thom SR; Bhopale VM; Velazquez OC; Goldstein LJ; Thom LH; Buerk DG. 2006. Stem cell mobilization by hyperbaric oxygen. Am J Physiol Heart Circ Physiol 290(4):H1378-86. [PubMed: 16299259]  [MGI Ref ID J:115770]

Tranguch S; Huet-Hudson Y. 2003. Decreased viability of nitric oxide synthase double knockout mice. Mol Reprod Dev 65(2):175-9. [PubMed: 12704728]  [MGI Ref ID J:83112]

Tsui AK; Marsden PA; Mazer CD; Adamson SL; Henkelman RM; Ho JJ; Wilson DF; Heximer SP; Connelly KA; Bolz SS; Lidington D; El-Beheiry MH; Dattani ND; Chen KM; Hare GM. 2011. Priming of hypoxia-inducible factor by neuronal nitric oxide synthase is essential for adaptive responses to severe anemia. Proc Natl Acad Sci U S A 108(42):17544-9. [PubMed: 21976486]  [MGI Ref ID J:177441]

Upmacis RK; Crabtree MJ; Deeb RS; Shen H; Lane PB; Benguigui LE; Maeda N; Hajjar DP; Gross SS. 2007. Profound biopterin oxidation and protein tyrosine nitration in tissues of ApoE-null mice on an atherogenic diet: contribution of inducible nitric oxide synthase. Am J Physiol Heart Circ Physiol 293(5):H2878-87. [PubMed: 17766468]  [MGI Ref ID J:132084]

Van Vliet BN; Chafe LL; Montani JP. 2003. Characteristics of 24 h telemetered blood pressure in eNOS-knockout and C57Bl/6J control mice. J Physiol 549(Pt 1):313-25. [PubMed: 12665600]  [MGI Ref ID J:105366]

Vandsburger MH; French BA; Kramer CM; Zhong X; Epstein FH. 2012. Displacement-encoded and manganese-enhanced cardiac MRI reveal that nNOS, not eNOS, plays a dominant role in modulating contraction and calcium influx in the mammalian heart. Am J Physiol Heart Circ Physiol 302(2):H412-9. [PubMed: 22058155]  [MGI Ref ID J:181655]

Vaporidi K; Francis RC; Bloch KD; Zapol WM. 2010. Nitric oxide synthase 3 contributes to ventilator-induced lung injury. Am J Physiol Lung Cell Mol Physiol 299(2):L150-9. [PubMed: 20453164]  [MGI Ref ID J:163364]

Vettor R; Valerio A; Ragni M; Trevellin E; Granzotto M; Olivieri M; Tedesco L; Ruocco C; Fossati A; Fabris R; Serra R; Carruba MO; Nisoli E. 2014. Exercise training boosts eNOS-dependent mitochondrial biogenesis in mouse heart: role in adaptation of glucose metabolism. Am J Physiol Endocrinol Metab 306(5):E519-28. [PubMed: 24381004]  [MGI Ref ID J:211616]

Wang CH; Li F; Hiller S; Kim HS; Maeda N; Smithies O; Takahashi N. 2011. A modest decrease in endothelial NOS in mice comparable to that associated with human NOS3 variants exacerbates diabetic nephropathy. Proc Natl Acad Sci U S A 108(5):2070-5. [PubMed: 21245338]  [MGI Ref ID J:169115]

Wang H; Kohr MJ; Traynham CJ; Ziolo MT. 2009. Phosphodiesterase 5 restricts NOS3/Soluble guanylate cyclase signaling to L-type Ca2+ current in cardiac myocytes. J Mol Cell Cardiol 47(2):304-14. [PubMed: 19345227]  [MGI Ref ID J:151357]

Wang H; Kohr MJ; Wheeler DG; Ziolo MT. 2008. Endothelial nitric oxide synthase decreases {beta}-adrenergic responsiveness via inhibition of the L-type Ca2+ current. Am J Physiol Heart Circ Physiol 294(3):H1473-80. [PubMed: 18203845]  [MGI Ref ID J:132621]

Wang T. 2002. Role of iNOS and eNOS in modulating proximal tubule transport and acid-base balance. Am J Physiol Renal Physiol 283(4):F658-62. [PubMed: 12217856]  [MGI Ref ID J:113614]

Wang T; Inglis FM; Kalb RG. 2000. Defective fluid and HCO(3)(-) absorption in proximal tubule of neuronal nitric oxide synthase-knockout mice. Am J Physiol Renal Physiol 279(3):F518-24. [PubMed: 10966931]  [MGI Ref ID J:64896]

Wang W; Mitra A; Poole B; Falk S; Lucia MS; Tayal S; Schrier R. 2004. Endothelial nitric oxide synthase-deficient mice exhibit increased susceptibility to endotoxin-induced acute renal failure. Am J Physiol Renal Physiol 287(5):F1044-8. [PubMed: 15475535]  [MGI Ref ID J:95428]

Wang WZ; Jones AW; Wang M; Durante W; Korthuis RJ. 2013. Preconditioning with soluble guanylate cyclase activation prevents postischemic inflammation and reduces nitrate tolerance in heme oxygenase-1 knockout mice. Am J Physiol Heart Circ Physiol 305(4):H521-32. [PubMed: 23771693]  [MGI Ref ID J:202294]

Wang Y; Ahmad N; Kudo M; Ashraf M. 2004. Contribution of Akt and endothelial nitric oxide synthase to diazoxide-induced late preconditioning. Am J Physiol Heart Circ Physiol 287(3):H1125-31. [PubMed: 15142844]  [MGI Ref ID J:95593]

Wegiel B; Gallo D; Csizmadia E; Roger T; Kaczmarek E; Harris C; Zuckerbraun BS; Otterbein LE. 2011. Biliverdin inhibits Toll-like receptor-4 (TLR4) expression through nitric oxide-dependent nuclear translocation of biliverdin reductase. Proc Natl Acad Sci U S A 108(46):18849-54. [PubMed: 22042868]  [MGI Ref ID J:180223]

Whiteus C; Freitas C; Grutzendler J. 2014. Perturbed neural activity disrupts cerebral angiogenesis during a postnatal critical period. Nature 505(7483):407-11. [PubMed: 24305053]  [MGI Ref ID J:207919]

Whiting C; Castillo A; Haque MZ; Majid DS. 2013. Protective role of the endothelial isoform of nitric oxide synthase in ANG II-induced inflammatory responses in the kidney. Am J Physiol Renal Physiol 305(7):F1031-41. [PubMed: 23926180]  [MGI Ref ID J:202044]

Wu M; Tsirka SE. 2009. Endothelial NOS-deficient mice reveal dual roles for nitric oxide during experimental autoimmune encephalomyelitis. Glia 57(11):1204-15. [PubMed: 19170181]  [MGI Ref ID J:156206]

Xuan YT; Guo Y; Zhu Y; Wang OL; Rokosh G; Bolli R. 2007. Endothelial nitric oxide synthase plays an obligatory role in the late phase of ischemic preconditioning by activating the protein kinase C epsilon p44/42 mitogen-activated protein kinase pSer-signal transducers and activators of transcription1/3 pathway. Circulation 116(5):535-44. [PubMed: 17606840]  [MGI Ref ID J:139855]

Yagi S; Aihara K; Ikeda Y; Sumitomo Y; Yoshida S; Ise T; Iwase T; Ishikawa K; Azuma H; Akaike M; Matsumoto T. 2008. Pitavastatin, an HMG-CoA reductase inhibitor, exerts eNOS-independent protective actions against angiotensin II induced cardiovascular remodeling and renal insufficiency. Circ Res 102(1):68-76. [PubMed: 17967781]  [MGI Ref ID J:145596]

Yamaguchi T; Kamada K; Dayton C; Gaskin FS; Yusof M; Yoshikawa T; Carter P; Korthuis RJ. 2007. Role of eNOS-derived NO in the postischemic anti-inflammatory effects of antecedent ethanol ingestion in murine small intestine. Am J Physiol Heart Circ Physiol 292(3):H1435-42. [PubMed: 17098834]  [MGI Ref ID J:120585]

Yang JZ; Ajonuma LC; Rowlands DK; Tsang LL; Ho LS; Lam SY; Chen WY; Zhou CX; Chung YW; Cho CY; Tse JY; James AE; Chan HC. 2005. The role of inducible nitric oxide synthase in gamete interaction and fertilization: a comparative study on knockout mice of three NOS isoforms. Cell Biol Int 29(9):785-91. [PubMed: 16087361]  [MGI Ref ID J:112824]

Yang XP; Liu YH; Shesely EG; Bulagannawar M; Liu F; Carretero OA. 1999. Endothelial nitric oxide gene knockout mice: cardiac phenotypes and the effect of angiotensin-converting enzyme inhibitor on myocardial ischemia/reperfusion injury. Hypertension 34(1):24-30. [PubMed: 10406819]  [MGI Ref ID J:57364]

Yang Z; Wang ZE; Doulias PT; Wei W; Ischiropoulos H; Locksley RM; Liu L. 2010. Lymphocyte Development Requires S-nitrosoglutathione Reductase. J Immunol 185(11):6664-9. [PubMed: 20980633]  [MGI Ref ID J:166150]

Yazji I; Sodhi CP; Lee EK; Good M; Egan CE; Afrazi A; Neal MD; Jia H; Lin J; Ma C; Branca MF; Prindle T; Richardson WM; Ozolek J; Billiar TR; Binion DG; Gladwin MT; Hackam DJ. 2013. Endothelial TLR4 activation impairs intestinal microcirculatory perfusion in necrotizing enterocolitis via eNOS-NO-nitrite signaling. Proc Natl Acad Sci U S A 110(23):9451-6. [PubMed: 23650378]  [MGI Ref ID J:197450]

Ye H; Charpin-El Hamri G; Zwicky K; Christen M; Folcher M; Fussenegger M. 2013. Pharmaceutically controlled designer circuit for the treatment of the metabolic syndrome. Proc Natl Acad Sci U S A 110(1):141-6. [PubMed: 23248313]  [MGI Ref ID J:192622]

Yokoyama M; Okada S; Nakagomi A; Moriya J; Shimizu I; Nojima A; Yoshida Y; Ichimiya H; Kamimura N; Kobayashi Y; Ohta S; Fruttiger M; Lozano G; Minamino T. 2014. Inhibition of endothelial p53 improves metabolic abnormalities related to dietary obesity. Cell Rep 7(5):1691-703. [PubMed: 24857662]  [MGI Ref ID J:211787]

Yu J; Zhang Y; Zhang X; Rudic RD; Bauer PM; Altieri DC; Sessa WC. 2012. Endothelium derived nitric oxide synthase negatively regulates the PDGF-survivin pathway during flow-dependent vascular remodeling. PLoS One 7(2):e31495. [PubMed: 22355372]  [MGI Ref ID J:185226]

Yu J; deMuinck ED; Zhuang Z; Drinane M; Kauser K; Rubanyi GM; Qian HS; Murata T; Escalante B; Sessa WC. 2005. Endothelial nitric oxide synthase is critical for ischemic remodeling, mural cell recruitment, and blood flow reserve. Proc Natl Acad Sci U S A 102(31):10999-1004. [PubMed: 16043715]  [MGI Ref ID J:100484]

Yusof M; Kamada K; Kalogeris T; Gaskin FS; Korthuis RJ. 2009. Hydrogen sulfide triggers late-phase preconditioning in postischemic small intestine by an NO- and p38 MAPK-dependent mechanism. Am J Physiol Heart Circ Physiol 296(3):H868-76. [PubMed: 19168723]  [MGI Ref ID J:146878]

Zhang M; Takimoto E; Lee DI; Santos CX; Nakamura T; Hsu S; Jiang A; Nagayama T; Bedja D; Yuan Y; Eaton P; Shah AM; Kass DA. 2012. Pathological cardiac hypertrophy alters intracellular targeting of phosphodiesterase type 5 from nitric oxide synthase-3 to natriuretic peptide signaling. Circulation 126(8):942-51. [PubMed: 22829024]  [MGI Ref ID J:202198]

Zhang YH; Zhang MH; Sears CE; Emanuel K; Redwood C; El-Armouche A; Kranias EG; Casadei B. 2008. Reduced phospholamban phosphorylation is associated with impaired relaxation in left ventricular myocytes from neuronal NO synthase-deficient mice. Circ Res 102(2):242-9. [PubMed: 18007024]  [MGI Ref ID J:141557]

Zhao HJ; Wang S; Cheng H; Zhang MZ; Takahashi T; Fogo AB; Breyer MD; Harris RC. 2006. Endothelial nitric oxide synthase deficiency produces accelerated nephropathy in diabetic mice. J Am Soc Nephrol 17(10):2664-9. [PubMed: 16971655]  [MGI Ref ID J:135864]

Zhao X; Chen YR; He G; Zhang A; Druhan LJ; Strauch AR; Zweier JL. 2007. Endothelial nitric oxide synthase (NOS3) knockout decreases NOS2 induction, limiting hyperoxygenation and conferring protection in the postischemic heart. Am J Physiol Heart Circ Physiol 292(3):H1541-50. [PubMed: 17114245]  [MGI Ref ID J:120584]

Zhao X; He G; Chen YR; Pandian RP; Kuppusamy P; Zweier JL. 2005. Endothelium-derived nitric oxide regulates postischemic myocardial oxygenation and oxygen consumption by modulation of mitochondrial electron transport. Circulation 111(22):2966-72. [PubMed: 15939832]  [MGI Ref ID J:112252]

Zhao X; Lu X; Feng Q. 2002. Deficiency in endothelial nitric oxide synthase impairs myocardial angiogenesis. Am J Physiol Heart Circ Physiol 283(6):H2371-8. [PubMed: 12388304]  [MGI Ref ID J:108272]

Zhao YY; Zhao YD; Mirza MK; Huang JH; Potula HH; Vogel SM; Brovkovych V; Yuan JX; Wharton J; Malik AB. 2009. Persistent eNOS activation secondary to caveolin-1 deficiency induces pulmonary hypertension in mice and humans through PKG nitration. J Clin Invest 119(7):2009-18. [PubMed: 19487814]  [MGI Ref ID J:152579]

Zhou Y; Mitra S; Varadharaj S; Parinandi N; Zweier JL; Flavahan NA. 2006. Increased expression of cyclooxygenase-2 mediates enhanced contraction to endothelin ETA receptor stimulation in endothelial nitric oxide synthase knockout mice. Circ Res 98(11):1439-45. [PubMed: 16645140]  [MGI Ref ID J:122612]

Zhou Y; Varadharaj S; Zhao X; Parinandi N; Flavahan NA; Zweier JL. 2005. Acetylcholine causes endothelium-dependent contraction of mouse arteries. Am J Physiol Heart Circ Physiol 289(3):H1027-32. [PubMed: 15879486]  [MGI Ref ID J:115427]

Zhu X; Liu B; Zhou S; Chen YR; Deng Y; Zweier JL; He G. 2007. Ischemic preconditioning prevents in vivo hyperoxygenation in postischemic myocardium with preservation of mitochondrial oxygen consumption. Am J Physiol Heart Circ Physiol 293(3):H1442-50. [PubMed: 17513495]  [MGI Ref ID J:126163]

Zuckerbraun BS; Chin BY; Wegiel B; Billiar TR; Czsimadia E; Rao J; Shimoda L; Ifedigbo E; Kanno S; Otterbein LE. 2006. Carbon monoxide reverses established pulmonary hypertension. J Exp Med 203(9):2109-19. [PubMed: 16908624]  [MGI Ref ID J:124569]

de Jonge WJ; Hallemeesch MM; Kwikkers KL; Ruijter JM; de Gier-de Vries C; van Roon MA; Meijer AJ; Marescau B; de Deyn PP; Deutz NE; Lamers WH. 2002. Overexpression of arginase I in enterocytes of transgenic mice elicits a selective arginine deficiency and affects skin, muscle, and lymphoid development. Am J Clin Nutr 76(1):128-40. [PubMed: 12081826]  [MGI Ref ID J:80556]

de Jonge WJ; Kwikkers KL; te Velde AA; van Deventer SJ; Nolte MA; Mebius RE; Ruijter JM; Lamers MC; Lamers WH. 2002. Arginine deficiency affects early B cell maturation and lymphoid organ development in transgenic mice. J Clin Invest 110(10):1539-48. [PubMed: 12438451]  [MGI Ref ID J:80204]

van Der Heyde HC; Gu Y; Zhang Q; Sun G; Grisham MB. 2000. Nitric oxide is neither necessary nor sufficient for resolution of plasmodium chabaudi malaria in mice J Immunol 165(6):3317-23. [PubMed: 10975849]  [MGI Ref ID J:64564]

van der Heijden OW; Essers YP; Fazzi G; Peeters LL; De Mey JG; van Eys GJ. 2005. Uterine artery remodeling and reproductive performance are impaired in endothelial nitric oxide synthase-deficient mice. Biol Reprod 72(5):1161-8. [PubMed: 15659709]  [MGI Ref ID J:104639]

Health & husbandry

Health & Colony Maintenance Information

Animal Health Reports

Room Number           AX1

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice are bred as homozygotes (by homozygous sibling matings).
Mating SystemHomozygote x Homozygote         (Female x Male)   01-MAR-06
Breeding Considerations This strain is a challenging breeder.
Diet Information LabDiet® 5K52/5K67

Pricing and Purchasing

Pricing, Supply Level & Notes, Controls


Pricing for USA, Canada and Mexico shipping destinations View International Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $104.70Female or MaleHomozygous for Nos3tm1Unc  
4 weeks $104.70Female or MaleHomozygous for Nos3tm1Unc  
5 weeks $104.70Female or MaleHomozygous for Nos3tm1Unc  
6 weeks $110.15Female or MaleHomozygous for Nos3tm1Unc  
7 weeks $115.60Female or MaleHomozygous for Nos3tm1Unc  
8 weeks $121.05Female or MaleHomozygous for Nos3tm1Unc  
9 weeks $126.50Female or MaleHomozygous for Nos3tm1Unc  
10 weeks $131.95Female or MaleHomozygous for Nos3tm1Unc  
11 weeks $137.40Female or MaleHomozygous for Nos3tm1Unc  
12 weeks $142.85Female or MaleHomozygous for Nos3tm1Unc  
Price per Pair (US dollars $)Pair Genotype
$220.30Homozygous for Nos3tm1Unc x Homozygous for Nos3tm1Unc  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
Pricing for International shipping destinations View USA Canada and Mexico Pricing

Live Mice

Weeks of AgePrice per mouse (US dollars $)GenderGenotypes Provided
3 weeks $136.20Female or MaleHomozygous for Nos3tm1Unc  
4 weeks $136.20Female or MaleHomozygous for Nos3tm1Unc  
5 weeks $136.20Female or MaleHomozygous for Nos3tm1Unc  
6 weeks $143.20Female or MaleHomozygous for Nos3tm1Unc  
7 weeks $150.30Female or MaleHomozygous for Nos3tm1Unc  
8 weeks $157.40Female or MaleHomozygous for Nos3tm1Unc  
9 weeks $164.50Female or MaleHomozygous for Nos3tm1Unc  
10 weeks $171.60Female or MaleHomozygous for Nos3tm1Unc  
11 weeks $178.70Female or MaleHomozygous for Nos3tm1Unc  
12 weeks $185.80Female or MaleHomozygous for Nos3tm1Unc  
Price per Pair (US dollars $)Pair Genotype
$286.40Homozygous for Nos3tm1Unc x Homozygous for Nos3tm1Unc  

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Supply Notes

  • Pair Pricing: Price may vary depending on the age of the males and females available for shipment. The price displayed is for a male and female at six weeks of age.
  • Shipped at a specific age in weeks. Mice at a precise age in days, littermates and retired breeders are also available.
View USA Canada and Mexico Pricing View International Pricing

Standard Supply

Level 4. Up to 10 mice. Larger quantities or custom orders arranged upon request. Expected delivery up to one to three months.

Control Information

  Control
   000664 C57BL/6J
 
  Considerations for Choosing Controls
  Control Pricing Information for Genetically Engineered Mutant Strains.
 

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Terms are granted by individual review and stated on the customer invoice(s) and account statement. These transactions are payable in U.S. currency within the granted terms. Payment for services, products, shipping containers, and shipping costs that are rendered are expected within the payment terms indicated on the invoice or stated by contract. Invoices and account balances in arrears of stated terms may result in The Jackson Laboratory pursuing collection activities including but not limited to outside agencies and court filings.


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The Jackson Laboratory's Genotype Promise

The Jackson Laboratory has rigorous genetic quality control and mutant gene genotyping programs to ensure the genetic background of JAX® Mice strains as well as the genotypes of strains with identified molecular mutations. JAX® Mice strains are only made available to researchers after meeting our standards. However, the phenotype of each strain may not be fully characterized and/or captured in the strain data sheets. Therefore, we cannot guarantee a strain's phenotype will meet all expectations. To ensure that JAX® Mice will meet the needs of individual research projects or when requesting a strain that is new to your research, we suggest ordering and performing tests on a small number of mice to determine suitability for your particular project.
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JAX® Mice
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Terms of Use

Terms of Use


General Terms and Conditions


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General inquiries regarding Terms of Use

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phone:207-288-6470

JAX® Mice, Products & Services Conditions of Use

"MICE" means mouse strains, their progeny derived by inbreeding or crossbreeding, unmodified derivatives from mouse strains or their progeny supplied by The Jackson Laboratory ("JACKSON"). "PRODUCTS" means biological materials supplied by JACKSON, and their derivatives. "RECIPIENT" means each recipient of MICE, PRODUCTS, or services provided by JACKSON including each institution, its employees and other researchers under its control. MICE or PRODUCTS shall not be: (i) used for any purpose other than the internal research, (ii) sold or otherwise provided to any third party for any use, or (iii) provided to any agent or other third party to provide breeding or other services. Acceptance of MICE or PRODUCTS from JACKSON shall be deemed as agreement by RECIPIENT to these conditions, and departure from these conditions requires JACKSON's prior written authorization.

No Warranty

MICE, PRODUCTS AND SERVICES ARE PROVIDED “AS IS”. JACKSON EXTENDS NO WARRANTIES OF ANY KIND, EITHER EXPRESS, IMPLIED, OR STATUTORY, WITH RESPECT TO MICE, PRODUCTS OR SERVICES, INCLUDING ANY IMPLIED WARRANTY OF MERCHANTABILITY OR FITNESS FOR A PARTICULAR PURPOSE, OR ANY WARRANTY OF NON-INFRINGEMENT OF ANY PATENT, TRADEMARK, OR OTHER INTELLECTUAL PROPERTY RIGHTS.

In case of dissatisfaction for a valid reason and claimed in writing by a purchaser within ninety (90) days of receipt of mice, products or services, JACKSON will, at its option, provide credit or replacement for the mice or product received or the services provided.

No Liability

In no event shall JACKSON, its trustees, directors, officers, employees, and affiliates be liable for any causes of action or damages, including any direct, indirect, special, or consequential damages, arising out of the provision of MICE, PRODUCTS or services, including economic damage or injury to property and lost profits, and including any damage arising from acts or negligence on the part of JACKSON, its agents or employees. Unless prohibited by law, in purchasing or receiving MICE, PRODUCTS or services from JACKSON, purchaser or recipient, or any party claiming by or through them, expressly releases and discharges JACKSON from all such causes of action or damages, and further agrees to defend and indemnify JACKSON from any costs or damages arising out of any third party claims.

MICE and PRODUCTS are to be used in a safe manner and in accordance with all applicable governmental rules and regulations.

The foregoing represents the General Terms and Conditions applicable to JACKSON’s MICE, PRODUCTS or services. In addition, special terms and conditions of sale of certain MICE, PRODUCTS or services may be set forth separately in JACKSON web pages, catalogs, price lists, contracts, and/or other documents, and these special terms and conditions shall also govern the sale of these MICE, PRODUCTS and services by JACKSON, and by its licensees and distributors.

Acceptance of delivery of MICE, PRODUCTS or services shall be deemed agreement to these terms and conditions. No purchase order or other document transmitted by purchaser or recipient that may modify the terms and conditions hereof, shall be in any way binding on JACKSON, and instead the terms and conditions set forth herein, including any special terms and conditions set forth separately, shall govern the sale of MICE, PRODUCTS or services by JACKSON.


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