Strain Name:

D2.129P2(B6)-Apoetm1Unc/J

Stock Number:

007067

Availability:

Repository- Live
Mice homozygous for the Apoetm1Unc mutation on the DBA/2J background may be useful in studies of diet-induced obesity without diabetes, Alzheimer's Disease, neurodegeneration, atherosclerosis and hypercholesterolemia.

Description

Strain Information

Type Congenic; Mutant Strain; Targeted Mutation;
Additional information on Genetically Engineered and Mutant Mice.
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Mating SystemHeterozygote x Heterozygote         (Female x Male)   04-FEB-09
Specieslaboratory mouse
Background Strain C57BL/6
Donor Strain 129P2 via E14TG2a ES cell line
GenerationN6F1 (19-NOV-09)
 
Donating Investigator IMR Colony,   The Jackson Laboratory

Description
Mice homozygous for the Apoetm1Unc mutation show a marked increase in total plasma cholesterol levels that are unaffected by age or sex. Fatty streaks in the proximal aorta are found at 3 months of age. The lesions increase with age and progress to lesions with less lipid but more elongated cells, typical of a more advanced stage of pre-atherosclerotic lesion. Moderately increased triglyceride levels have been reported in mice with this mutation on a mixed C57BL/6 x 129 genetic background. Aged APOE deficient mice (>17 months) have been shown to develop xanthomatous lesions in the brain consisting mostly of crystalline cholesterol clefts, lipid globules, and foam cells. Smaller xanthomas were seen in the choroid plexus and ventral fornix. Recent studies indicate that APOE deficient mice have altered responses to stress, impaired spatial learning and memory, altered long term potentiation, and synaptic damage.

In an attempt to offer alleles on well-characterized or multiple genetic backgrounds, alleles are frequently moved to a genetic background different from that on which an allele was first characterized. This is the case for the strain above. It should be noted that the phenotype could vary from that originally described. We will modify the strain description if necessary as published results become available.

Development
The Apoetm1Unc mutant strain was developed in the laboratory of Dr. Nobuyo Maeda at The University of North Carolina at Chapel Hill. The 129-derived E14Tg2a ES cell line was used. The plasmid used is designated as pNMC109 and the founder line is T-89 in the primary reference. The mice were backcrossed to C57BL/6J for 10 generation and then backcrossed to DBA/2J for 5 generations (using a speed congenic protocol) before being made homozygous.

Control Information

  Control
   Wild-type from the colony
   000671 DBA/2J
 
  Considerations for Choosing Controls

Related Strains

View Strains carrying   Apoetm1Unc     (11 strains)

Strains carrying other alleles of Apoe
008525   B6.Cg-Tg(Cyp21a1-Apoe)619Fet/J
View Strains carrying other alleles of Apoe     (1 strain)

Additional Web Information

Visit the Alzheimer's Disease Mouse Model Resource site for helpful information on Alzheimer's Disease and research resources.

Phenotype

Phenotype Information

View Related Disease (OMIM) Terms

Related Disease (OMIM) Terms
Apolipoprotein E; APOE - Models with phenotypic similarity to human disease where etiologies involve orthologs.1
1 Human genes are associated with this disease. Orthologs of those genes appear in the mouse genotype(s).
View Mammalian Phenotype Terms

Mammalian Phenotype Terms
      assigned by genotype

The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.

Apoetm1Unc/Apoe+

        involves: 129P2/OlaHsd * C57BL/6
  • homeostasis/metabolism phenotype
  • increased circulating triglyceride level (MGI Ref ID J:16573)
    • circulating triglyceride levels are 39% higher than in wild-type controls

Apoetm1Unc/Apoetm1Unc

        B6.129P2-Apoetm1Unc/J
  • life span-post-weaning/aging
  • premature death (MGI Ref ID J:73202)
    • 35% dead by 18 months
  • cardiovascular system phenotype
  • abnormal aorta morphology (MGI Ref ID J:101576)
    • at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta
    • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
    • endothelial nitric oxide synthase (eNOS) in mutant aortic wall is distinctly reduced
    • Cx43 distribution at cell-cell junction shows significant disruption
  • abnormal blood flow velocity (MGI Ref ID J:108154)
    • anesthetized homozygotes show significantly increased transaortic blood velocities relative to wild-type mice with peak aortic velocity at 133.4 ± 7.8 cm/s vs 89.2 ± 5.8 cm/s, and mean aortic velocity at 35.9 ± 2.7 vs 22.0 ± 1.6 cm/s, respectively
    • in addition, anesthetized homozygotes show significantly increased transmitral blood velocities relative to wild-type mice with peak mitral velocities at 92 ± 7.2 cm/s vs 47.2 ± 5.3 cm/s, and mean mitral velocities at 20.6 ± 1.7 vs 11.4 ± 1.3 cm/s, respectively
    • no significant differences in heart rate, peak aortic acceleration or ejection time are observed in the conscious or anesthetized state, when normalized to body weight
    • however, homozygotes show alterations in aortic arch acceleration suggestive of increased peripheral wave reflections
  • abnormal blood vessel physiology (MGI Ref ID J:60364)
    • pulse wave velocity is insignificantly elevated at 4 months
    • pulse wave velocity significantly elevated at 13 months
    • abnormal blood-brain barrier function (MGI Ref ID J:69455)
      • impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex
    • atherosclerotic lesions (MGI Ref ID J:133606)
      • advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries
      • at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation
      • lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions
      • regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice
      • at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta
      • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
      • plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes
      • 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age
      • 61% covered by plaques at 13 months of age
      • thickened intima, foam cell accumulation and thin collagen cap
      • focal fragmentation of elastic laminae
      • intimal lesions are observed in atherosclerotic aortas in mutants
      • major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch
      • lesions comprise around 14-16% of total aortic arch area in male and female mutants
      • aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area
      • increased susceptibility to atherosclerosis (MGI Ref ID J:101576)
        • severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively
        • on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis
    • decreased vasodilation (MGI Ref ID J:101576)
      • homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice
    • vascular stenosis (MGI Ref ID J:101576)
      • vascular stenosis is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
      • spiral modiolar artery stenosis (MGI Ref ID J:101576)
        • lumen stenosis of the spiral modiolar artery in the cochlea is exacerbated by an atherosclerotic diet relative to a normal diet
  • abnormal cardiac stroke volume (MGI Ref ID J:108154)
    • under anesthesia, homozygotes appear to exhibit significantly increased stroke volume
  • abnormal spiral modiolar artery morphology (MGI Ref ID J:101576)
    • homozygotes fed an atherosclerotic diet develop atherosclerotic alterations in the spiral modiolar artery (SMA)
    • in contrast, no such changes are detected in the SMA of homozygotes fed a normal diet
  • arteriosclerosis (MGI Ref ID J:108154)
    • homozygotes exhibit a 13% increase in aortic pulse-wave velocity (PWV) relative to wild-type mice (428 ± 14.5 cm/s vs 379 ± 10.1 cm/s), indicating increased arterial stiffness and reduced vascular elasticity
    • atherosclerotic lesions (MGI Ref ID J:133606)
      • advanced atherosclerotic lesions; massive atheromas with abundant cholesterol crystals, neutral lipids, and diminished extracellular matrix in arotic roots and coronary arteries
      • at 13 months, homozygotes display atherosclerotic lesions extending from the carotid arteries, heart, and aorta down to the renal arteries and the iliac bifurcation
      • lesions are most severe in the proximal aorta and at the bifurcation of carotid arteries; the proximal carotid arteries are relatively free of lesions
      • regular exercise does not reduce atherosclerotic lesion formation in homozygotes, as shown by a comparable % oil red-O staining of whole aortas from sedentary and exercised mutant mice
      • at 24 weeks of age, homozygotes fed a normal diet (but not similarly-fed C57BL/6J control mice) show obvious atherosclerotic lesions in the aortic sinus and ascending aorta
      • the number of atherosclerotic lesions in aortic sinus and ascending aorta is significantly increased in homozygotes fed an atherosclerotic diet vs a normal diet
      • plaques in the luminal surface of the aorta are significantly larger in atherosclerotic diet homozygotes than in normal diet homozygotes
      • 23% of luminal surface in the aortic arch and thoracic aorta is covered by plaques at 4 months of age
      • 61% covered by plaques at 13 months of age
      • thickened intima, foam cell accumulation and thin collagen cap
      • focal fragmentation of elastic laminae
      • intimal lesions are observed in atherosclerotic aortas in mutants
      • major lesions are observed on lesser curvature of aortic arch in males and females with minor lesions found at branches of aortic arch
      • lesions comprise around 14-16% of total aortic arch area in male and female mutants
      • aortic lesions are observed in aortic sinus at level of aortic valve leaflets; lesions are about 27% of total aortal area
      • increased susceptibility to atherosclerosis (MGI Ref ID J:101576)
        • severity of atherosclerosis is 2-fold and 99-fold higher in atherosclerotic diet homozygotes than in normal diet homozygotes and C57BL/6J control mice, respectively
        • on a high fat, high cholesterol diet, mutants exhibit moderate to severe aortic and carotid atherosclerosis
  • cardiac hypertrophy (MGI Ref ID J:108154)
    • at 13 months, homozygotes show a 59% increase in heart weight-to-body weight ratio relative to wild-type mice
  • decreased systemic vascular resistance (MGI Ref ID J:108154)
    • under anesthesia, homozygotes appear to exhibit significantly reduced peripheral vascular resistance and compliance in the presence of normal blood pressures
  • increased cardiac output (MGI Ref ID J:108154)
    • under anesthesia, homozygotes exhibit elevated flow velocities suggesting elevated cardiac output
  • increased heart weight (MGI Ref ID J:108154)
    • at 13 months, homozygotes show a 23% increase in heart weight relative to wild-type mice (186 ± 7.1 vs. 151 ± 2.5 mg)
  • muscle phenotype
  • decreased vasodilation (MGI Ref ID J:101576)
    • homozygotes fed a normal or atherosclerotic diet show severely impaired endothelium-dependent relaxation to acetylcholine in aortic rings relative to age-matched C57BL/6J control mice
  • impaired muscle relaxation (MGI Ref ID J:60364)
    • relaxation response to acetylcholine in blood vessels is significantly attenuated at 13 months of age
    • maximal response to acetylcholine is considerably reduced
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level (MGI Ref ID J:73202)
    • decreased HDL/total cholesterol ratio
    • decreased HDL/LDL ratio
    • increased circulating cholesterol level (MGI Ref ID J:73202)
      • increasing with age; 4-fold increase in plasma total cholesterol levels in 10-12 week old mutants and 13-fold increase at 29 weeks
      • exercise (15 or 60 min/day swim) causes no significant changes in total cholesterol levels among homozygotes or wild-type mice relative to sedentary, genotype-matched controls
      • on a normal diet, homozygotes display significantly increased plasma total cholesterol (TC) levels relative to C57BL/6J control mice
      • on an atherosclerotic diet, homozygotes show a further significant increase in plasma TC levels relative to homozygotes on a normal diet
      • 5 fold increase in total cholesterol at 24 and 36 weeks
      • total serum cholesterol 70 fold higher than controls on a normal diet
      • total serum cholesterol 20 fold higher than controls on high fat diet where controls show 4 fold increase over normal diet
      • significantly increased relative to wild-type controls at 24 weeks of age; levels in mutants after induction of chronic graft versus host disease (cGVH) to induce systemic lupus erythematosus (SLE) are equivalent to the Apoe-null mice
      • increased circulating LDL cholesterol level (MGI Ref ID J:93987)
        • on a normal diet, homozygotes display significantly increased plasma LDL cholesterol levels relative to C57BL/6J control mice
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma LDL levels relative to homozygotes on a normal diet
      • increased circulating VLDL cholesterol level (MGI Ref ID J:93987)
        • on a normal diet, homozygotes display significantly increased plasma VLDL cholesterol levels relative to C57BL/6J control mice
        • on an atherosclerotic diet, homozygotes show a further significant increase in plasma VLDL cholesterol levels relative to homozygotes on a normal diet
  • abnormal circulating homocysteine level (MGI Ref ID J:73202)
    • decrease in plasma total homocysteine levels
  • abnormal enzyme/coenzyme activity (MGI Ref ID J:73202)
    • activity of cholesterol synthesis enzyme HMG-CoA reductase is reduced up to 60% in aging mice compared to 30% in wild-type aging mice
  • decreased circulating glucose level (MGI Ref ID J:73202)
  • decreased circulating triglyceride level (MGI Ref ID J:93987)
  • hyperlipidemia (MGI Ref ID J:101576)
    • homozygotes develop hyperlipidemia; however, HDL cholesterol levels, body weight and blood glucose remain unchanged relative to C57BL/6J control mice on a normal diet, with no further differences noted on an atheroscletoric diet
  • increased circulating triglyceride level (MGI Ref ID J:73202)
    • 2-fold increase in plasma triglyceride levels in 10-12 week old mutants
    • on a normal diet, homozygotes display significantly increased plasma triglyceride levels relative to C57BL/6J control mice
    • on an atherosclerotic diet, homozygotes show a further significant increase in plasma triglyceride levels relative to homozygotes on a normal diet
  • xanthoma (MGI Ref ID J:43846)
    • 1 of 11 aged mice on a normal diet develops cerebral xanthoma
    • eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components
  • skin/coat/nails phenotype
  • skin lesions (MGI Ref ID J:73202)
    • progressive skin lesions, mainly seen as eruptive xanthomas on shoulder and back areas with lipids and extracellular matix as the predominant components
  • growth/size phenotype
  • decreased body length (MGI Ref ID J:136630)
    • nose to rump length less than controls at both 1 and 3 months
  • decreased body weight (MGI Ref ID J:60364)
    • at 13 months, homozygotes show a 22% reduction in body weight relative to wild-type mice (34.5 ± 0.9 vs. 44.5 ± 1.1 g)
  • increased weight gain (MGI Ref ID J:136630)
    • body weight was less than controls at 3 months but identical at 8 months
  • hematopoietic system phenotype
  • abnormal B cell activation (MGI Ref ID J:133606)
    • spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23
  • abnormal T cell number (MGI Ref ID J:47027)
    • increased numbers of cytokine producing T cells
    • abnormal CD4-positive T cell number (MGI Ref ID J:108154)
      • clusters of CD4+ cells found in fatty streak lesions
      • ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet
      • increased T-helper 2 cell number (MGI Ref ID J:47027)
  • decreased follicular B cell number (MGI Ref ID J:133606)
    • decreased relative to controls
  • decreased hematocrit (MGI Ref ID J:108154)
    • at 13 months, awake, unanesthetized homozygotes display slightly but significantly reduced hematocrits ( 11%) relative to wild-type mice at 41.7 ± 1.1% vs 46.6 ± 0.4%; in contrast, systolic blood pressures remain unaffected (140 ± 7.6 mmHg vs 136 ± 7.4 mmHg)
  • decreased marginal zone B cell number (MGI Ref ID J:133606)
    • with induction of SLE by cGVH, levels are slightly decreased compared to wild-type
  • increased B cell number (MGI Ref ID J:133606)
    • newly formed B cells are significantly increased compared to wild-type
    • increased marginal zone B cell number (MGI Ref ID J:133606)
      • increased 2-fold compared to wild-type
  • increased spleen weight (MGI Ref ID J:61564)
    • increased spleen weight while the thymus weight remains normal
  • cellular phenotype
  • oxidative stress (MGI Ref ID J:97385)
    • regular exercise fails to reduce endogenous oxidant load and mitochondrial damage in hypercholesterolemic mutant mice
    • in contrast, regular exercise results in reduced mitochondrial damage and oxidant load and increased SOD2 and adenine nucleotide translocator activities in normocholesterolemic control mice
  • hearing/vestibular/ear phenotype
  • abnormal cochlea morphology (MGI Ref ID J:101576)
    • endothelial nitric oxide synthase (eNOS) in mutant cochlea is distinctly reduced
    • abnormal basilar membrane (MGI Ref ID J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic basilar membrane
    • abnormal stria vascularis (MGI Ref ID J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic stria vascularis
    • abnormal tectorial membrane morphology (MGI Ref ID J:101576)
      • on an atherosclerotic diet, homozygotes display a sclerosed and atrophic tectorial membrane
    • cochlear inner hair cell degeneration (MGI Ref ID J:101576)
      • at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn
      • IHC loss at the base turn is exacerbated by an atherosclerotic diet
    • cochlear outer hair cell degeneration (MGI Ref ID J:101576)
      • at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn
      • OHC loss at the base turn is exacerbated by an atherosclerotic diet
    • organ of Corti degeneration (MGI Ref ID J:101576)
      • at 24 weeks, homozygotes fed a normal diet show significant degeneration of the organ of Corti in the basal turn while the middle turn is relatively normal
      • degeneration of the organ of Corti is excerbated by an atherosclerotic diet, with complete loss noted in the basal turn in some animals
  • deafness (MGI Ref ID J:101576)
    • homozygotes fed a normal diet display hearing loss esp. at high frequencies as compared with C57BL/6J control mice
    • a high positive correlation between ABR thresholds at 16 and 8 kHz, or click and atherosclerotic lesions, and atherosclerotic plaque area of the aorta, and plasma total choelsterol levels is observed in both normal diet and high-fat diet homozygotes
  • decreased brainstem auditory evoked potential (MGI Ref ID J:101576)
    • at 10 weeks, homozygotes fed a normal diet display higher ABR thresholds than C57BL/6J control mice at all test frequencies, with more hearing loss noted at 32 kHz; by 24 weeks, further hearing loss is detected at all test stimuli levels
    • homozygotes fed an atherosclerotic diet show higher ABR thresholds than homozygotes fed a normal diet
  • nervous system phenotype
  • abnormal blood-brain barrier function (MGI Ref ID J:69455)
    • impaired blood-brain barrier and blood-nerve barrier as indicated by extensive extravasation of serum proteins into sciatic nerve, spinal cord and cerebellum and occasional extravasation into cortex and subcortex
  • cochlear ganglion degeneration (MGI Ref ID J:101576)
    • at 24 weeks, homozygotes fed a normal diet show a reduced number of spiral ganglion cells in the basal turn of the cochlea
    • loss of ganglion cells is excerbated by an atherosclerotic diet
  • cochlear inner hair cell degeneration (MGI Ref ID J:101576)
    • at 24 weeks, homozygotes fed a normal diet show almost complete loss of IHCs in the basal turn and some IHC loss in the middle turn
    • IHC loss at the base turn is exacerbated by an atherosclerotic diet
  • cochlear outer hair cell degeneration (MGI Ref ID J:101576)
    • at 24 weeks, homozygotes fed a normal diet show almost complete loss of OHCs in the basal turn and some OHC loss in the middle turn
    • OHC loss at the base turn is exacerbated by an atherosclerotic diet
  • immune system phenotype
  • abnormal immune system morphology (MGI Ref ID J:47027)
    • abnormal B cell activation (MGI Ref ID J:133606)
      • spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23
    • abnormal T cell number (MGI Ref ID J:47027)
      • increased numbers of cytokine producing T cells
      • abnormal CD4-positive T cell number (MGI Ref ID J:108154)
        • clusters of CD4+ cells found in fatty streak lesions
        • ratio of Th2 to Th1 cells is increased from 4.4 to 11.4 on a normal diet and up to 20.9 on a high cholesterol diet
        • increased T-helper 2 cell number (MGI Ref ID J:47027)
    • decreased follicular B cell number (MGI Ref ID J:133606)
      • decreased relative to controls
    • decreased marginal zone B cell number (MGI Ref ID J:133606)
      • with induction of SLE by cGVH, levels are slightly decreased compared to wild-type
    • increased B cell number (MGI Ref ID J:133606)
      • newly formed B cells are significantly increased compared to wild-type
      • increased marginal zone B cell number (MGI Ref ID J:133606)
        • increased 2-fold compared to wild-type
    • increased spleen weight (MGI Ref ID J:61564)
      • increased spleen weight while the thymus weight remains normal
  • abnormal immune system physiology (MGI Ref ID J:61564)
    • abnormal B cell activation (MGI Ref ID J:133606)
      • spleen cells display polyclonal B cell activation, with increased expression of MHC II, Fas, and CD86 and lower expression of CD21, CD22, and CD23
    • abnormal immune serum protein physiology (MGI Ref ID J:61564)
      • decreased interferon-gamma secretion (MGI Ref ID J:47027)
        • production is reduced when fed a high cholesterol diet
      • increased immunoglobulin level (MGI Ref ID J:133606)
        • mutants with cGVH-induced SLE show greatly increased levels compared to wild-type controls or untreated mutants
        • increased IgM level (MGI Ref ID J:61564)
          • IgM response to tetanus toxoid is significantly increased as compared to controls
    • decreased susceptibility to type IV hypersensitivity reaction (MGI Ref ID J:61564)
      • decreased antigen specific delayed hypersensitivity response
    • increased autoantibody level (MGI Ref ID J:133606)
      • after induction of cGVH-SLE, IgG and IgM anti-oxidized LDL and anti-cardiolipin antibodies are increased compared to wild-type or Apoe-null controls
      • increased anti-nuclear antigen antibody level (MGI Ref ID J:133606)
        • after induction of cGVH-SLE, mice display greatly increased levels of anti-chromatin antibodies compared to wild-type controls or non-cGVH mutants
        • increased anti-double stranded DNA antibody level (MGI Ref ID J:133606)
          • after induction of cGVH-SLE, mice display greatly increased levels compared to wild-type controls or non-cGVH-SLE mutants
    • increased susceptibility to systemic lupus erythematosus (MGI Ref ID J:133606)
  • behavior/neurological phenotype
  • abnormal spatial learning (MGI Ref ID J:120203)
    • longer latency to find the platform in Morris maze tests
    • slow to acquire a preference for the target quadrant and the magnitude of the preference is always less than controls
  • increased thigmotaxis (MGI Ref ID J:120203)
    • elevated thigmotaxis in Morris maze tests
  • renal/urinary system phenotype
  • abnormal renal glomerulus morphology (MGI Ref ID J:125978)
    • glomerular foam cells in the mesangium, capillary lumina and within the glomerular stalk close to the vascular pole
    • lipid deposits in arteriolar walls in the vascular poles
    • lipid droplets filling glomerular capillary lumina at 36 weeks in about 50% of mice
    • loss of mesangial matrix sometimes at 36 weeks but never at 24 weeks or in controls
    • increased glomerular tuft area
    • glomerular cell numbers are increased
  • liver/biliary system phenotype
  • abnormal liver physiology (MGI Ref ID J:104609)
    • no significant change in serum alanine transaminase with high fat diet as is seen in controls (marker for liver damage)
    • hepatic uptake of LDL is increased two fold
  • vision/eye phenotype
  • abnormal eye electrophysiology (MGI Ref ID J:84688)
    • implicit times increased for a and b waves of dark adapted electroretinogram
    • wave amplitudes attenuated for a and b waves of dark adapted electroretinogram
  • abnormal retinal inner nuclear layer morphology (MGI Ref ID J:70245)
    • perinuclear vacuolation on a high cholesterol diet
    • thin retinal inner nuclear layer (MGI Ref ID J:70245)
      • cell numbers reduced
  • thin retinal outer nuclear layer (MGI Ref ID J:70245)
    • cell numbers reduced
  • taste/olfaction phenotype
  • impaired olfaction (MGI Ref ID J:89344)
    • preference for plain water over 0.1% iso-amyl alcohol moderate compared to the strong preference shown by controls
    • slower than control to find buried food pellet although found pellets visually more rapidly
    • latency to taste vanillin-cued quinine significantly increased only at day 5
  • skeleton phenotype
  • abnormal bone structure (MGI Ref ID J:111209)
    • abnormal cancellous bone morphology (MGI Ref ID J:111209)
      • increased number of trabeculae
    • increased bone density (MGI Ref ID J:111209)
      • higher bone mineralization density in vertebral bodies
      • increased bone volume to tissue volume ratio
    • increased cortical bone thickness (MGI Ref ID J:111209)
      • in vertebral bodies and tibia
  • abnormal skeleton physiology (MGI Ref ID J:111209)
    • abnormal osteoblast physiology (MGI Ref ID J:111209)
      • increased rate of bone formation
  • respiratory system phenotype
  • abnormal respiratory alveoli morphology (MGI Ref ID J:136630)
    • fewer but larger alveoli at 3 months of age
    • less surface area to volume
  • abnormal respiratory function (MGI Ref ID J:136630)
    • percent increase in hysteresivity with age greater than in controls
    • abnormal airway resistance (MGI Ref ID J:136630)
      • resistance to airflow greater than controls at 3months but not at 8 months
    • abnormal lung capacity (MGI Ref ID J:136630)
      • lung volume similar to controls at 3months but 2.5 fold greater at 8 months
    • abnormal lung compliance (MGI Ref ID J:136630)
      • dynamic and static compliance greater than controls at 8 months

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd * C57BL/6
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:80689)
    • greater than in wild-type
    • fatty streaks with foam cells are found in the proximal aorta of 3-8 month old mice fed normal chow
    • the foam cells are often adjacent to valve attachment sites and can form multi-layers
    • lesions get bigger with age and near total occlusion at the entrance of a coronary artery can be observed at 8 months of age
    • 75% of mice develop lesions in the aortic arch with most females and some males having calcification within the lesions
    • aortic cartilaginous metaplasia is noted in the most severely affected mice
  • homeostasis/metabolism phenotype
  • decreased circulating HDL cholesterol level (MGI Ref ID J:16573)
    • mean HDL levels (33 mg/dl) are 45% of that found in controls
  • hyperlipidemia (MGI Ref ID J:80689)
    • relative to wild-type
  • increased circulating cholesterol level (MGI Ref ID J:80689)
    • relative to wild-type
    • mean total cholesterol levels are elevated about 5-fold over wild-type to 434 mg/dl
    • total cholesterol levels are about 4-fold higher than controls with a mean of 379 mg/dl
    • increased circulating LDL cholesterol level (MGI Ref ID J:16573)
      • mice have elevated levels of LDL in the blood
    • increased circulating VLDL cholesterol level (MGI Ref ID J:16573)
      • the majority of lipoprotein particles in the blood are in the VLDL size range
  • increased circulating triglyceride level (MGI Ref ID J:80689)
    • relative to wild-type
    • circulating triglyceride levels are 123 mg/dl compared to 73 mg/dl in controls
  • increased prostaglandin level (MGI Ref ID J:125376)
    • amount of PGE2 in aortas is 4X higher than in controls
    • PGE2 level doubles on a high fat diet
  • nervous system phenotype
  • abnormal glial cell physiology (MGI Ref ID J:58019)
    • astrocytes secrete less phospholipids or free cholesterol compared to wild-type astrocytes
  • abnormal synapse morphology (MGI Ref ID J:43043)
    • elevated cholesterol in the exofacial leaflet of the synaptic plasma membrane but not so high as for Ldlr deficient mice
    • cholesterol levels in the cytofacial leaflet are reduced

Apoetm1Unc/Apoetm1Unc

        either: B6.129P2-Apoetm1Unc/J or (involves: 129P2/OlaHsd * C57BL/6J * ICR)
  • behavior/neurological phenotype
  • *normal* behavior/neurological phenotype (MGI Ref ID J:100975)
    • no alterations in passive avoidance learning are observed; coordination levels measured in rotorod tests are similar to wild-type
    • abnormal spatial learning (MGI Ref ID J:100975)
      • 6-month old female mice show subtle learning impairment in water maze task compared to transgenic mutants; 6-month old males show significantly decreased learning ability in the Morris water maze test
    • decreased vertical activity (MGI Ref ID J:100975)
      • mice have fewer rearing events and shorter rearing times than wild-type controls
  • nervous system phenotype
  • *normal* nervous system phenotype (MGI Ref ID J:100975)
    • mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus mice exhibit age-dependent loss of synaptophysin-reactive terminals and microtubule-associated protein 2-positive neuronal dendrites in the neocortex and hippocampus, similar to wild-type
    • upon 18 mg/kg kainic acid injection, significant loss of neocortical synaptophysin-positive presynaptic terminals and disruption of hippocampal axons are observed, similar to wild-type
    • mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months) mice show significant loss of synaptophysin-positive presynaptic terminals and neuronal dendrites of the neocortex and hippocampus with age (7-9 months compared to 3-4 months), similar to wild-type

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd
  • behavior/neurological phenotype
  • increased anxiety-related response (MGI Ref ID J:101973)
    • in the elevated-plus maze, mice show increased anxiety with reduced time and distance moved in the open arms; mice have significantly lower number of open-arm entries than wild-type
    • effect is age-dependent; phenotype is present in older mice, but not in young 2-4 month-old mice
  • increased startle reflex (MGI Ref ID J:101973)
    • response is higher in mice at 6 months of age compared to wild-type
  • hearing/vestibular/ear phenotype
  • increased startle reflex (MGI Ref ID J:101973)
    • response is higher in mice at 6 months of age compared to wild-type
  • homeostasis/metabolism phenotype
  • abnormal circulating cholesterol level (MGI Ref ID J:48202)
    • circulating VLDL/LDL cholesterol levels are increased compared to in Apobec1tm1Chan homozygotes and wild-type mice
    • increased circulating cholesterol level (MGI Ref ID J:48202)
      • when fed a chow or Western-type diet for 2 weeks, mice exhibit increased serum cholesterol compared with Apobec1tm1Chan homozygotes and wild-type mice
  • decreased cerebral infarction size (MGI Ref ID J:133156)
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice
  • increased circulating corticosterone level (MGI Ref ID J:101973)
    • all males have higher plasma concentrations than wild-type after behavioral testing
  • nervous system phenotype
  • abnormal dendrite morphology (MGI Ref ID J:101973)
    • mutants have lower levels of MAP 2-positive neuronal dendrites than wild-type; at 3 months, levels are similar in mutants and controls
  • decreased cerebral infarction size (MGI Ref ID J:133156)
    • compared to in Tg(Eno2-APP751)10Cord Apoetm1Unc/Apoetm1Unc mice
  • cardiovascular system phenotype
  • increased susceptibility to atherosclerosis (MGI Ref ID J:107390)
    • bone marrow transplanted into Apoa1tm1Unc homozygotes confer susceptibility to atherosclerosis

Apoetm1Unc/Apoetm1Unc

        B6.129P2-Apoetm1Unc
  • immune system phenotype
  • abnormal cell-mediated immunity (MGI Ref ID J:125366)
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
    • in an adoptive transfer experiment, the proliferation of Tg(TcrLCMV)2Aox CD45.2+ cell in mice fed a high fat diet and receiving then immunized with GP61-80 peptide with CpG is reduced compared to in wild-type mice similarly treated
    • abnormal dendritic cell physiology (MGI Ref ID J:125366)
      • dendrictic cells mount reduced IL-12p40 and TNF-alpha responses to stimulation with zymosan, poly(I:C), LPS, imiquimod, and a combination of anti-CD40 antibodies and CpG compared to wild-type mice but similar to wild-type mice fed a high fat diet
      • in mice fed a high fat diet, dendritic cell production of IL-12p40, IL-6 and TNF-alpha after 35 to 40 weeks, but not after 6 to 10 weeks, is severely impaired compared to wild-type cells in response to CpG/anti-CD-40 stimulation
      • CD8alpha-, but not CD8alpha+, dendritic cells are defective in their ability to produce IL-12p40
      • dendritic cells from mice on a high fat diet are severely impaired in their ability to produce Il-12p40, -12p70, -6, and TNF-alpha compared to dendritic cells from wild-type mice on a high fat diet
      • however, CD8alpha+ dendritic cells produce normal amounts of Il-12p70 and -12p40
      • mice fed a high fat diet and co-stimulated with CpG or LPS have fewer IL-12p40-producing CD8alpha- dendritic cells (4.6+/-1.1%) than wild-type mice fed a high fat diet (15.3+/-2.4%)
      • however, the immune responses of bone marrow derived dendritic cells from mice fed a high fat diet or splenic dendritic cells from mice fed a regular diet are normal
  • increased CD4-positive T cell number (MGI Ref ID J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice
  • increased susceptibility to parasitic infection (MGI Ref ID J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major produce more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice
    • the immune response of mice fed a high fat diet to Leishmania major infection is skewed towards a Th2-type response
    • mice maintained on a high fat diet or regular chow and infect with Leishmania major exhibit an increased swelling and parasitic burden at the site of infection (footpad)
  • homeostasis/metabolism phenotype
  • abnormal lipid level (MGI Ref ID J:125366)
    • mice have increased levels of circulating oxidized lipids compared to wild-type mice
    • increased circulating cholesterol level (MGI Ref ID J:61287)
      • mice develop severe cholesterolemia when receiving a high fat diet from 6 to 30 weeks (elevated levels are detected at 6, 15, and 30 weeks)
  • decreased circulating leptin level (MGI Ref ID J:60585)
    • plasma leptin levels are low at both 6 and 18 months
  • behavior/neurological phenotype
  • abnormal eating/drinking behavior (MGI Ref ID J:60585)
    • increased drinking behavior (MGI Ref ID J:60585)
      • increased water intake at 18 months
    • increased eating behavior (MGI Ref ID J:60585)
      • increased food intake at 12 and 18 months but not earlier
  • abnormal kindling response (MGI Ref ID J:118390)
    • after-discharge duration is significantly prolonged by the sixth trial
    • delayed rekindling after 3-4 weeks
  • abnormal locomotor activity (MGI Ref ID J:71062)
    • mice spend more time than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc in the center of an open field
  • abnormal response to new environment (MGI Ref ID J:71062)
    • mice consume food slower in a new environment than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc and wild-type mice
    • mice require more time to habituate to a novel environment compared to wild-type mice
    • mice are less reluctant than wild-type mice to move into an open area
    • decreased exploration in new environment (MGI Ref ID J:60585)
      • reduced exploratory behavior in an open field test by 12 months although normal earlier
      • exploratory behavior remains constant over several days whereas controls show higher initial exploratory behavior which drops off quickly
  • abnormal spatial learning (MGI Ref ID J:71062)
    • at 14 to 17 months of age, mice perform better than Tg(GFAP-APOE*4)Hol Apoetm1Unc/Apoetm1Unc and wild-type mice in a rotating holeboard test
  • abnormal thermal nociception (MGI Ref ID J:106368)
    • 41% increase in foot withdrawal latency from painful thermal stimuli
    • 100% slower tail withdrawal latency
  • decreased startle reflex (MGI Ref ID J:71062)
  • increased anxiety-related response (MGI Ref ID J:60585)
    • at 6 months as measured in an elevated plus maze
  • hearing/vestibular/ear phenotype
  • decreased startle reflex (MGI Ref ID J:71062)
  • hematopoietic system phenotype
  • increased CD4-positive T cell number (MGI Ref ID J:125366)
    • mice maintained on a high fat diet and infect with Leishmania major generate more IL-4 and IL-5 producing CD4+ T cells compared to wild-type mice
  • nervous system phenotype
  • abnormal kindling response (MGI Ref ID J:118390)
    • after-discharge duration is significantly prolonged by the sixth trial
    • delayed rekindling after 3-4 weeks
  • abnormal myelin sheath morphology (MGI Ref ID J:106368)
    • very little Schwann cell cytoplasm
    • blurring of lipid membrane border between axons and Schwann cells
  • abnormal sciatic nerve (MGI Ref ID J:106368)
    • cross-section of unmyelinated axons is irregular
    • very little Schwann cell cytoplasm
    • blurring of lipid membrane border between axons and Schwann cells
    • reduced number of unmyelinated axons
    • ratio of unmyelinated to myelinated axons is reduced
  • abnormal synaptic vesicle morphology (MGI Ref ID J:118390)
    • synaptophysin levels are somewhat more reduced than in controls after entorhinal cortex lesion
  • hypopituitarism (MGI Ref ID J:60585)
    • restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels
  • touch/vibrissae phenotype
  • abnormal thermal nociception (MGI Ref ID J:106368)
    • 41% increase in foot withdrawal latency from painful thermal stimuli
    • 100% slower tail withdrawal latency
  • endocrine/exocrine gland phenotype
  • abnormal adrenal gland morphology (MGI Ref ID J:60585)
    • abnormal adrenal cortex morphology (MGI Ref ID J:60585)
      • increased lipid droplets seen at six months
    • abnormal adrenal medulla morphology (MGI Ref ID J:60585)
      • increased lipid droplets seen at six months
  • abnormal gland physiology (MGI Ref ID J:60585)
    • hypersecretion of corticosterone (MGI Ref ID J:60585)
      • fter 10 min of restraint stress plasma levels are elevated at six months but not at three months
      • elevated adrenal levels at six months but not earlier
    • hypopituitarism (MGI Ref ID J:60585)
      • restraint stress at 6 months results in disproportionately low ACTH levels as compared to plasma corticosterone levels
  • adipose tissue phenotype
  • decreased brown adipose tissue amount (MGI Ref ID J:60585)
    • decreased interscapular brown fat at 18 but not at 6 months
  • decreased white adipose tissue amount (MGI Ref ID J:60585)
    • epididymal white fat reduced at both 6 and 18 months
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:61287)
    • cellular composition of lesions is similar among Serpine1-deficient or transgenic, Apoe-deficient genotypes, or Apoe-deficient only mice; at early time points, a greater foam cell content is observed, with more prominent cholesterol clefts and necrotic areas evident with increasing age

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd * 129S4/SvJae * C57BL/6
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:66419)
    • most severe in the aortic arch region

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd * C57BL/6 * FVB/N
  • cardiovascular system phenotype
  • atherosclerotic lesions (MGI Ref ID J:130658)
    • lesions are observed in aortas of nontransgenic mice

Apoetm1Unc/Apoetm1Unc

        involves: 129P2/OlaHsd * C57BL/6 * DBA
  • homeostasis/metabolism phenotype
  • abnormal circulating protein level (MGI Ref ID J:75567)
    • increase in APOB-48
  • abnormal lipid homeostasis (MGI Ref ID J:75567)
    • the HDL phospholipid fraction is enriched in 16:0 and 18:0 species and contains less 20:4 and 22:6 species compared to Ldlrtm1Her single mutants
    • abnormal cholesterol homeostasis (MGI Ref ID J:75567)
      • increase in the APOB lipoprotein cholesterol level compared to wild-type controls
      • there is a 2.3 fold increase in the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species compared to Ldlrtm1Her single mutants
      • the ratio of saturated + monounsaturated/polyunsaturated cholesterol ester fatty acid species in the LDL fraction is significantly increased compared to Ldlrtm1Her single mutants
      • decreased circulating HDL cholesterol level (MGI Ref ID J:75567)
        • about a 50% decrease in HDL compared to controls
      • increased circulating cholesterol level (MGI Ref ID J:75567)
        • increased total cholesterol and esterfied cholesterol levels in the plasma
    • increased circulating phospholipid level (MGI Ref ID J:75567)
View Research Applications

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

Diabetes and Obesity Research
Obesity Without Diabetes
      diet-induced

Neurobiology Research
Alzheimer's Disease
      APOE mutants
Behavioral and Learning Defects
Neurodegeneration

Apoetm1Unc related

Cardiovascular Research
Atherosclerosis
Hypercholesterolemia

Mouse/Human Gene Homologs
Alzheimer's
hyperlipoproteinemia, type III

Genes & Alleles

Gene & Allele Information

 
Allele Symbol Apoetm1Unc
Allele Name targeted mutation 1, University of North Carolina
Allele Type Targeted (knock-out)
Common Name(s) APOE KO; AopE(-); ApoE-KO; Apoetm1Un; apoE-; apoE0; epsilon-;
Mutation Made By Nobuyo Maeda,   Univ of North Carolina at Chapel Hill
Strain of Origin129P2/OlaHsd
ES Cell Line NameE14TG2a
ES Cell Line Strain129P2/OlaHsd
Gene Symbol and Name Apoe, apolipoprotein E
Chromosome 7
Gene Common Name(s) AD2; AI255918; APOEA; LDLCQ5; LPG; MGC1571; expressed sequence AI255918;
Molecular Note Insertion of a neomycin resistance cassette deleted part of exon 3 and part of intron 3 of the Apoe gene. Plasma from homozygous mutant mice gave no detectable immunoprecipitate by the Ouchterlony double immunodiffusion test using a rabbit antibody to rat APOE. [MGI Ref ID J:1050]

Genotyping

Genotyping Information

Genotyping Protocols

Apoetm1Unc, Standard PCR

Helpful Links

Genotyping resources and troubleshooting

References

References

Selected Reference(s)

Piedrahita JA; Zhang SH; Hagaman JR; Oliver PM; Maeda N. 1992. Generation of mice carrying a mutant apolipoprotein E gene inactivated by gene targeting in embryonic stem cells. Proc Natl Acad Sci U S A 89(10):4471-5. [PubMed: 1584779]  [MGI Ref ID J:1050]

Additional References

Apoetm1Unc related

't Hoen PA; Van der Lans CA; Van Eck M; Bijsterbosch MK; Van Berkel TJ; Twisk J. 2003. Aorta of ApoE-deficient mice responds to atherogenic stimuli by a prelesional increase and subsequent decrease in the expression of antioxidant enzymes. Circ Res 93(3):262-9. [PubMed: 12829615]  [MGI Ref ID J:115676]

A-Gonzalez N; Bensinger SJ; Hong C; Beceiro S; Bradley MN; Zelcer N; Deniz J; Ramirez C; Diaz M; Gallardo G; de Galarreta CR; Salazar J; Lopez F; Edwards P; Parks J; Andujar M; Tontonoz P; Castrillo A. 2009. Apoptotic cells promote their own clearance and immune tolerance through activation of the nuclear receptor LXR. Immunity 31(2):245-58. [PubMed: 19646905]  [MGI Ref ID J:151872]

Accad M; Smith SJ; Newland DL; Sanan DA; King LE Jr; Linton MF; Fazio S; Farese RV Jr. 2000. Massive xanthomatosis and altered composition of atherosclerotic lesions in hyperlipidemic mice lacking acyl CoA:cholesterol acyltransferase 1 [see comments] J Clin Invest 105(6):711-9. [PubMed: 10727439]  [MGI Ref ID J:61147]

Adachi H; Fujiwara Y; Kondo T; Nishikawa T; Ogawa R; Matsumura T; Ishii N; Nagai R; Miyata K; Tabata M; Motoshima H; Furukawa N; Tsuruzoe K; Kawashima J; Takeya M; Yamashita S; Koh GY; Nagy A; Suda T; Oike Y; Araki E. 2009. Angptl 4 deficiency improves lipid metabolism, suppresses foam cell formation and protects against atherosclerosis. Biochem Biophys Res Commun 379(4):806-11. [PubMed: 19094966]  [MGI Ref ID J:145171]

Agrawal S; Febbraio M; Podrez E; Cathcart MK; Stark GR; Chisolm GM. 2007. Signal transducer and activator of transcription 1 is required for optimal foam cell formation and atherosclerotic lesion development. Circulation 115(23):2939-47. [PubMed: 17533179]  [MGI Ref ID J:137115]

Ahluwalia N; Lin AY; Tager AM; Pruitt IE; Anderson TJ; Kristo F; Shen D; Cruz AR; Aikawa M; Luster AD; Gerszten RE. 2007. Inhibited aortic aneurysm formation in BLT1-deficient mice. J Immunol 179(1):691-7. [PubMed: 17579092]  [MGI Ref ID J:143153]

Aihara K; Azuma H; Akaike M; Ikeda Y; Sata M; Takamori N; Yagi S; Iwase T; Sumitomo Y; Kawano H; Yamada T; Fukuda T; Matsumoto T; Sekine K; Sato T; Nakamichi Y; Yamamoto Y; Yoshimura K; Watanabe T; Nakamura T; Oomizu A; Tsukada M; Hayashi H; Sudo T; KatoS; Matsumoto T. 2007. Strain-dependent embryonic lethality and exaggerated vascular remodeling in heparin cofactor II-deficient mice. J Clin Invest 117(6):1514-26. [PubMed: 17549254]  [MGI Ref ID J:122173]

Aikawa E; Nahrendorf M; Sosnovik D; Lok VM; Jaffer FA; Aikawa M; Weissleder R. 2007. Multimodality molecular imaging identifies proteolytic and osteogenic activities in early aortic valve disease. Circulation 115(3):377-86. [PubMed: 17224478]  [MGI Ref ID J:130156]

Alexander MR; Knowles JW; Nishikimi T; Maeda N. 2003. Increased atherosclerosis and smooth muscle cell hypertrophy in natriuretic peptide receptor A-/-apolipoprotein E-/- mice. Arterioscler Thromb Vasc Biol 23(6):1077-82. [PubMed: 12702516]  [MGI Ref ID J:103054]

Ali K; Middleton M; Pure E; Rader DJ. 2005. Apolipoprotein E suppresses the type I inflammatory response in vivo. Circ Res 97(9):922-7. [PubMed: 16179587]  [MGI Ref ID J:114634]

Alp NJ; McAteer MA; Khoo J; Choudhury RP; Channon KM. 2004. Increased endothelial tetrahydrobiopterin synthesis by targeted transgenic GTP-cyclohydrolase I overexpression reduces endothelial dysfunction and atherosclerosis in ApoE-knockout mice. Arterioscler Thromb Vasc Biol 24(3):445-50. [PubMed: 14707037]  [MGI Ref ID J:102062]

Amar S; Wu SC; Madan M. 2009. Is Porphyromonas gingivalis cell invasion required for atherogenesis? Pharmacotherapeutic implications. J Immunol 182(3):1584-92. [PubMed: 19155507]  [MGI Ref ID J:144322]

Amigo L; Quinones V; Mardones P; Zanlungo S; Miquel JF; Nervi F; Rigotti A. 2000. Impaired biliary cholesterol secretion and decreased gallstone formation in apolipoprotein E-deficient mice fed a high-cholesterol diet. Gastroenterology 118(4):772-9. [PubMed: 10734029]  [MGI Ref ID J:107676]

An G; Miwa T; Song WL; Lawson JA; Rader DJ; Zhang Y; Song WC. 2009. CD59 but not DAF deficiency accelerates atherosclerosis in female ApoE knockout mice. Mol Immunol 46(8-9):1702-9. [PubMed: 19297024]  [MGI Ref ID J:148359]

Anderson DR; Tsutsui JM; Xie F; Radio SJ; Porter TR. 2007. The role of complement in the adherence of microbubbles to dysfunctional arterial endothelium and atherosclerotic plaque. Cardiovasc Res 73(3):597-606. [PubMed: 17196951]  [MGI Ref ID J:119533]

Anderson R; Barnes JC; Bliss TV; Cain DP; Cambon K; Davies HA; Errington ML; Fellows LA; Gray RA; Hoh T; Stewart M; Large CH; Higgins GA. 1998. Behavioural, physiological and morphological analysis of a line of apolipoprotein E knockout mouse. Neuroscience 85(1):93-110. [PubMed: 9607706]  [MGI Ref ID J:118390]

Anderson R; Higgins GA. 1997. Absence of central cholinergic deficits in ApoE knockout mice. Psychopharmacology (Berl) 132(2):135-44. [PubMed: 9266610]  [MGI Ref ID J:127860]

Andersson IJ; Jiang YY; Davidge ST. 2009. Maternal stress and development of atherosclerosis in the adult apolipoprotein E-deficient mouse offspring. Am J Physiol Regul Integr Comp Physiol 296(3):R663-71. [PubMed: 19129374]  [MGI Ref ID J:145701]

Ando Y; Shimizugawa T; Takeshita S; Ono M; Shimamura M; Koishi R; Furukawa H. 2003. A decreased expression of angiopoietin-like 3 is protective against atherosclerosis in apoE-deficient mice. J Lipid Res 44(6):1216-23. [PubMed: 12671033]  [MGI Ref ID J:84022]

Angeli V; Llodra J; Rong JX; Satoh K; Ishii S; Shimizu T; Fisher EA; Randolph GJ. 2004. Dyslipidemia associated with atherosclerotic disease systemically alters dendritic cell mobilization. Immunity 21(4):561-74. [PubMed: 15485633]  [MGI Ref ID J:93917]

Aprahamian T; Bonegio R; Rizzo J; Perlman H; Lefer DJ; Rifkin IR; Walsh K. 2006. Simvastatin treatment ameliorates autoimmune disease associated with accelerated atherosclerosis in a murine lupus model. J Immunol 177(5):3028-34. [PubMed: 16920939]  [MGI Ref ID J:139547]

Aprahamian T; Bonegio RG; Richez C; Yasuda K; Chiang LK; Sato K; Walsh K; Rifkin IR. 2009. The peroxisome proliferator-activated receptor gamma agonist rosiglitazone ameliorates murine lupus by induction of adiponectin. J Immunol 182(1):340-6. [PubMed: 19109165]  [MGI Ref ID J:142895]

Aprahamian T; Rifkin I; Bonegio R; Hugel B; Freyssinet JM; Sato K; Castellot JJ Jr; Walsh K. 2004. Impaired Clearance of Apoptotic Cells Promotes Synergy between Atherogenesis and Autoimmune Disease. J Exp Med 199(8):1121-31. [PubMed: 15096538]  [MGI Ref ID J:91058]

Atkinson RD; Coenen KR; Plummer MR; Gruen ML; Hasty AH. 2008. Macrophage-derived apolipoprotein E ameliorates dyslipidemia and atherosclerosis in obese apolipoprotein E-deficient mice. Am J Physiol Endocrinol Metab 294(2):E284-90. [PubMed: 18029445]  [MGI Ref ID J:133332]

Auger A; Truong TQ; Rhainds D; Lapointe J; Letarte F; Brissette L. 2001. Low and high density lipoprotein metabolism in primary cultures of hepatic cells from normal and apolipoprotein E knockout mice. Eur J Biochem 268(8):2322-30. [PubMed: 11298750]  [MGI Ref ID J:115588]

Azuma K; Ichimura K; Mita T; Nakayama S; Jin WL; Hirose T; Fujitani Y; Sumiyoshi K; Shimada K; Daida H; Sakai T; Mitsumata M; Kawamori R; Watada H. 2009. Presence of alpha-smooth muscle actin-positive endothelial cells in the luminal surface of adult aorta. Biochem Biophys Res Commun 380(3):620-6. [PubMed: 19285011]  [MGI Ref ID J:147062]

Babaev VR; Ding L; Reese J; Morrow JD; Breyer MD; Dey SK; Fazio S; Linton MF. 2006. Cyclooxygenase-1 deficiency in bone marrow cells increases early atherosclerosis in apolipoprotein E- and low-density lipoprotein receptor-null mice. Circulation 113(1):108-17. [PubMed: 16380543]  [MGI Ref ID J:121507]

Baldan A; Pei L; Lee R; Tarr P; Tangirala RK; Weinstein MM; Frank J; Li AC; Tontonoz P; Edwards PA. 2006. Impaired development of atherosclerosis in hyperlipidemic Ldlr-/- and ApoE-/- mice transplanted with Abcg1-/- bone marrow. Arterioscler Thromb Vasc Biol 26(10):2301-7. [PubMed: 16888235]  [MGI Ref ID J:128048]

Bales KR; Liu F; Wu S; Lin S; Koger D; DeLong C; Hansen JC; Sullivan PM; Paul SM. 2009. Human APOE isoform-dependent effects on brain beta-amyloid levels in PDAPP transgenic mice. J Neurosci 29(21):6771-9. [PubMed: 19474305]  [MGI Ref ID J:149522]

Bales KR; Verina T; Cummins DJ; Du Y; Dodel RC; Saura J; Fishman CE; DeLong CA; Piccardo P; Petegnief V; Ghetti B; Paul SM. 1999. Apolipoprotein E is essential for amyloid deposition in the APP(V717F) transgenic mouse model of Alzheimer's disease. Proc Natl Acad Sci U S A 96(26):15233-8. [PubMed: 10611368]  [MGI Ref ID J:59078]

Bales KR; Verina T; Dodel RC; Du Y; Altstiel L; Bender M; Hyslop P; Johnstone EM; Little SP; Cummins DJ; Piccardo P; Ghetti B; Paul SM. 1997. Lack of apolipoprotein E dramatically reduces amyloid beta-peptide deposition [letter] [see comments] Nat Genet 17(3):263-4. [PubMed: 9354781]  [MGI Ref ID J:43845]

Barile GR; Pachydaki SI; Tari SR; Lee SE; Donmoyer CM; Ma W; Rong LL; Buciarelli LG; Wendt T; Horig H; Hudson BI; Qu W; Weinberg AD; Yan SF; Schmidt AM. 2005. The RAGE axis in early diabetic retinopathy. Invest Ophthalmol Vis Sci 46(8):2916-24. [PubMed: 16043866]  [MGI Ref ID J:103714]

Barlic J; Murphy PM. 2007. Chemokine regulation of atherosclerosis. J Leukoc Biol 82(2):226-36. [PubMed: 17329566]  [MGI Ref ID J:123530]

Barry-Lane PA; Patterson C; van der Merwe M; Hu Z; Holland SM; Yeh ET; Runge MS. 2001. p47phox is required for atherosclerotic lesion progression in ApoE(-/-) mice. J Clin Invest 108(10):1513-22. [PubMed: 11714743]  [MGI Ref ID J:111638]

Barton M; Haudenschild CC; d'Uscio LV; Shaw S; Munter K; Luscher TF. 1998. Endothelin ETA receptor blockade restores NO-mediated endothelial function and inhibits atherosclerosis in apolipoprotein E-deficient mice. Proc Natl Acad Sci U S A 95(24):14367-72. [PubMed: 9826706]  [MGI Ref ID J:51282]

Bates KA; Fonte J; Robertson TA; Martins RN; Harvey AR. 2002. Chronic gliosis triggers Alzheimer's disease-like processing of amyloid precursor protein. Neuroscience 113(4):785-96. [PubMed: 12182886]  [MGI Ref ID J:120711]

Baumgartl J; Baudler S; Scherner M; Babaev V; Makowski L; Suttles J; McDuffie M; Tobe K; Kadowaki T; Fazio S; Kahn CR; Hotamisligil GS; Krone W; Linton M; Bruning JC. 2006. Myeloid lineage cell-restricted insulin resistance protects apolipoproteinE-deficient mice against atherosclerosis. Cell Metab 3(4):247-56. [PubMed: 16581002]  [MGI Ref ID J:129654]

Bechtholt AJ; Smith R; Raber J; Cunningham CL. 2004. Enhanced ethanol-, but not cocaine-induced, conditioned place preference in Apoe(-/-) mice. Pharmacol Biochem Behav 77(4):783-92. [PubMed: 15099924]  [MGI Ref ID J:102259]

Beckers L; Heeneman S; Wang L; Burkly L; Rousch M; Davidson N; Gijbels M; de Winther M; Daemen M; Lutgens E. 2007. Disruption of hedgehog signalling in ApoE - /- mice reduces plasma lipid levels, but increases atherosclerosis due to enhanced lipid uptake by macrophages. J Pathol 212(4):420-8. [PubMed: 17573667]  [MGI Ref ID J:122864]

Bengtsson E; To F; Hakansson K; Grubb A; Branen L; Nilsson J; Jovinge S. 2005. Lack of the cysteine protease inhibitor cystatin C promotes atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 25(10):2151-6. [PubMed: 16051881]  [MGI Ref ID J:114346]

Bennett BJ; Scatena M; Kirk EA; Rattazzi M; Varon RM; Averill M; Schwartz SM; Giachelli CM; Rosenfeld ME. 2006. Osteoprotegerin inactivation accelerates advanced atherosclerotic lesion progression and calcification in older ApoE-/- mice. Arterioscler Thromb Vasc Biol 26(9):2117-24. [PubMed: 16840715]  [MGI Ref ID J:128053]

Bentzon JF; Sondergaard CS; Kassem M; Falk E. 2007. Smooth muscle cells healing atherosclerotic plaque disruptions are of local, not blood, origin in apolipoprotein E knockout mice. Circulation 116(18):2053-61. [PubMed: 17938286]  [MGI Ref ID J:142997]

Berbee JF; van der Hoogt CC; Sundararaman D; Havekes LM; Rensen PC. 2005. Severe hypertriglyceridemia in human APOC1 transgenic mice is caused by apoC-I-induced inhibition of LPL. J Lipid Res 46(2):297-306. [PubMed: 15576844]  [MGI Ref ID J:96691]

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Westerterp M; Berbee JF; Pires NM; van Mierlo GJ; Kleemann R; Romijn JA; Havekes LM; Rensen PC. 2007. Apolipoprotein C-I is crucially involved in lipopolysaccharide-induced atherosclerosis development in apolipoprotein E-knockout mice. Circulation 116(19):2173-81. [PubMed: 17967778]  [MGI Ref ID J:142992]

Westrick RJ; Bodary PF; Xu Z; Shen YC; Broze GJ; Eitzman DT. 2001. Deficiency of tissue factor pathway inhibitor promotes atherosclerosis and thrombosis in mice. Circulation 103(25):3044-6. [PubMed: 11425765]  [MGI Ref ID J:103352]

Whitman SC; Ravisankar P; Daugherty A. 2002. Interleukin-18 enhances atherosclerosis in apolipoprotein E(-/-) mice through release of interferon-gamma. Circ Res 90(2):E34-8. [PubMed: 11834721]  [MGI Ref ID J:109710]

Willner EL; Tow B; Buhman KK; Wilson M; Sanan DA; Rudel LL; Farese RV Jr. 2003. Deficiency of acyl CoA:cholesterol acyltransferase 2 prevents atherosclerosis in apolipoprotein E-deficient mice. Proc Natl Acad Sci U S A 100(3):1262-7. [PubMed: 12538880]  [MGI Ref ID J:81836]

Wilson KM; McCaw RB; Leo L; Arning E; Lhotak S; Bottiglieri T; Austin RC; Lentz SR. 2007. Prothrombotic effects of hyperhomocysteinemia and hypercholesterolemia in ApoE-deficient mice. Arterioscler Thromb Vasc Biol 27(1):233-40. [PubMed: 17082485]  [MGI Ref ID J:147558]

Wilson PG; Thompson JC; Webb NR; de Beer FC; King VL; Tannock LR. 2008. Serum amyloid A, but not C-reactive protein, stimulates vascular proteoglycan synthesis in a pro-atherogenic manner. Am J Pathol 173(6):1902-10. [PubMed: 18974302]  [MGI Ref ID J:143924]

Witting PK; Pettersson K; Ostlund-Lindqvist AM; Westerlund C; Eriksson AW; Stocker R. 1999. Inhibition by a coantioxidant of aortic lipoprotein lipid peroxidation and atherosclerosis in apolipoprotein E and low density lipoprotein receptor gene double knockout mice. FASEB J 13(6):667-75. [PubMed: 10094927]  [MGI Ref ID J:54037]

Wolfsgruber W; Feil S; Brummer S; Kuppinger O; Hofmann F; Feil R. 2003. A proatherogenic role for cGMP-dependent protein kinase in vascular smooth muscle cells. Proc Natl Acad Sci U S A 100(23):13519-24. [PubMed: 14597716]  [MGI Ref ID J:128779]

Wong CW; Christen T; Roth I; Chadjichristos CE; Derouette JP; Foglia BF; Chanson M; Goodenough DA; Kwak BR. 2006. Connexin37 protects against atherosclerosis by regulating monocyte adhesion. Nat Med 12(8):950-4. [PubMed: 16862155]  [MGI Ref ID J:111966]

Woollett LA; Osono Y; Herz J; Dietschy JM. 1995. Apolipoprotein E competitively inhibits receptor-dependent low density lipoprotein uptake by the liver but has no effect on cholesterol absorption or synthesis in the mouse. Proc Natl Acad Sci U S A 92(26):12500-4. [PubMed: 8618929]  [MGI Ref ID J:30297]

Wright SD; Burton C; Hernandez M; Hassing H; Montenegro J; Mundt S; Patel S; Card DJ; Hermanowski-Vosatka A; Bergstrom JD; Sparrow CP; Detmers PA; Chao YS. 2000. Infectious agents are not necessary for murine atherogenesis. J Exp Med 191(8):1437-42. [PubMed: 10770809]  [MGI Ref ID J:61722]

Wu BJ; Kathir K; Witting PK; Beck K; Choy K; Li C; Croft KD; Mori TA; Tanous D; Adams MR; Lau AK; Stocker R. 2006. Antioxidants protect from atherosclerosis by a heme oxygenase-1 pathway that is independent of free radical scavenging. J Exp Med 203(4):1117-27. [PubMed: 16606673]  [MGI Ref ID J:123780]

Wu D; Sharan C; Yang H; Goodwin JS; Zhou L; Grabowski GA; Du H; Guo Z. 2007. Apolipoprotein E-deficient lipoproteins induce foam cell formation by downregulation of lysosomal hydrolases in macrophages. J Lipid Res 48(12):2571-8. [PubMed: 17720994]  [MGI Ref ID J:129977]

Wu D; Yang H; Xiang W; Zhou L; Shi M; Julies G; Laplante JM; Ballard BR; Guo Z. 2005. Heterozygous mutation of ataxia-telangiectasia mutated gene aggravates hypercholesterolemia in apoE-deficient mice. J Lipid Res 46(7):1380-7. [PubMed: 15863839]  [MGI Ref ID J:100500]

Wu JH; Goswami R; Cai X; Exum ST; Huang X; Zhang L; Brian L; Premont RT; Peppel K; Freedman NJ. 2006. Regulation of the platelet-derived growth factor receptor-beta by G protein-coupled receptor kinase-5 in vascular smooth muscle cells involves the phosphatase Shp2. J Biol Chem 281(49):37758-72. [PubMed: 17018529]  [MGI Ref ID J:117638]

Wuttge DM; Eriksson P; Sirsjo A; Hansson GK; Stemme S. 2001. Expression of interleukin-15 in mouse and human atherosclerotic lesions. Am J Pathol 159(2):417-23. [PubMed: 11485899]  [MGI Ref ID J:70860]

Xian X; Ding Y; Zhang L; Wang Y; McNutt MA; Ross C; Hayden MR; Deng X; Liu G. 2009. Enhanced atherothrombotic formation after oxidative injury by FeCl3 to the common carotid artery in severe combined hyperlipidemic mice. Biochem Biophys Res Commun 385(4):563-9. [PubMed: 19481534]  [MGI Ref ID J:151434]

Xiao N; Yin M; Zhang L; Qu X; Du H; Sun X; Mao L; Ren G; Zhang C; Geng Y; An L; Pan J. 2009. Tumor necrosis factor-alpha deficiency retards early fatty-streak lesion by influencing the expression of inflammatory factors in apoE-null mice. Mol Genet Metab 96(4):239-44. [PubMed: 19157944]  [MGI Ref ID J:146902]

Xie C; Burns DK; Turley SD; Dietschy JM. 2000. Cholesterol is sequestered in the brains of mice with Niemann-Pick type C disease but turnover is increased. J Neuropathol Exp Neurol 59(12):1106-17. [PubMed: 11138930]  [MGI Ref ID J:104996]

Xu F; Ji J; Li L; Chen R; Hu WC. 2007. Adventitial fibroblasts are activated in the early stages of atherosclerosis in the apolipoprotein E knockout mouse. Biochem Biophys Res Commun 352(3):681-8. [PubMed: 17141183]  [MGI Ref ID J:116614]

Xu PT; Schmechel D; Rothrock-Christian T; Burkhart DS; Qiu HL; Popko B; Sullivan P; Maeda N; Saunders AM; Roses AD; Gilbert JR. 1996. Human apolipoprotein E2, E3, and E4 isoform-specific transgenic mice: human-like pattern of glial and neuronal immunoreactivity in central nervous system not observed in wild-type mice. Neurobiol Dis 3(3):229-45. [PubMed: 8980023]  [MGI Ref ID J:109197]

Yagyu H; Ishibashi S; Chen Z; Osuga J; Okazaki M; Perrey S; Kitamine T; Shimada M; Ohashi K; Harada K; Shionoiri F; Yahagi N; Gotoda T; Yazaki Y; Yamada N. 1999. Overexpressed lipoprotein lipase protects against atherosclerosis in apolipoprotein E knockout mice. J Lipid Res 40(9):1677-85. [PubMed: 10484615]  [MGI Ref ID J:57257]

Yagyu H; Kitamine T; Osuga J; Tozawa R; Chen Z; Kaji Y; Oka T; Perrey S; Tamura Y; Ohashi K; Okazaki H; Yahagi N; Shionoiri F; Iizuka Y; Harada K; Shimano H; Yamashita H; Gotoda T; Yamada N; Ishibashi S. 2000. Absence of ACAT-1 attenuates atherosclerosis but causes dry eye and cutaneous xanthomatosis in mice with congenital hyperlipidemia. J Biol Chem 275(28):21324-30. [PubMed: 10777503]  [MGI Ref ID J:63468]

Yamauchi T; Kamon J; Waki H; Imai Y; Shimozawa N; Hioki K; Uchida S; Ito Y; Takakuwa K; Matsui J; Takata M; Eto K; Terauchi Y; Komeda K; Tsunoda M; Murakami K; Ohnishi Y; Naitoh T; Yamamura K; Ueyama Y; Froguel P; Kimura S; Nagai R; Kadowaki T. 2003. Globular adiponectin protected ob/ob mice from diabetes and ApoE-deficient mice from atherosclerosis. J Biol Chem 278(4):2461-8. [PubMed: 12431986]  [MGI Ref ID J:81727]

Yancey PG; Jerome WG; Yu H; Griffin EE; Cox BE; Babaev VR; Fazio S; Linton MF. 2007. Severely altered cholesterol homeostasis in macrophages lacking apoE and SR-BI. J Lipid Res 48(5):1140-9. [PubMed: 17299204]  [MGI Ref ID J:121848]

Yang H; Roberts LJ; Shi MJ; Zhou LC; Ballard BR; Richardson A; Guo ZM. 2004. Retardation of atherosclerosis by overexpression of catalase or both Cu/Zn-superoxide dismutase and catalase in mice lacking apolipoprotein E. Circ Res 95(11):1075-81. [PubMed: 15528470]  [MGI Ref ID J:103561]

Yang J; Sato K; Aprahamian T; Brown NJ; Hutcheson J; Bialik A; Perlman H; Walsh K. 2004. Endothelial overexpression of Fas ligand decreases atherosclerosis in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 24(8):1466-73. [PubMed: 15178561]  [MGI Ref ID J:102307]

Yao J; Petanceska SS; Montine TJ; Holtzman DM; Schmidt SD; Parker CA; Callahan MJ; Lipinski WJ; Bisgaier CL; Turner BA; Nixon RA; Martins RN; Ouimet C; Smith JD; Davies P; Laska E; Ehrlich ME; Walker LC; Mathews PM; Gandy S. 2004. Aging, gender and APOE isotype modulate metabolism of Alzheimer's Abeta peptides and F-isoprostanes in the absence of detectable amyloid deposits. J Neurochem 90(4):1011-8. [PubMed: 15287908]  [MGI Ref ID J:107867]

Yet SF; Layne MD; Liu X; Chen YH; Ith B; Sibinga NE; Perrella MA. 2003. Absence of heme oxygenase-1 exacerbates atherosclerotic lesion formation and vascular remodeling. FASEB J 17(12):1759-61. [PubMed: 12958201]  [MGI Ref ID J:85417]

Yi X; Maeda N. 2006. alpha-Lipoic acid prevents the increase in atherosclerosis induced by diabetes in apolipoprotein E-deficient mice fed high-fat/low-cholesterol diet. Diabetes 55(8):2238-44. [PubMed: 16873686]  [MGI Ref ID J:116519]

Yoshimatsu M; Terasaki Y; Sakashita N; Kiyota E; Sato H; van der Laan LJ; Takeya M. 2004. Induction of macrophage scavenger receptor MARCO in nonalcoholic steatohepatitis indicates possible involvement of endotoxin in its pathogenic process. Int J Exp Pathol 85(6):335-43. [PubMed: 15566430]  [MGI Ref ID J:104609]

Yoshimura K; Aoki H; Ikeda Y; Fujii K; Akiyama N; Furutani A; Hoshii Y; Tanaka N; Ricci R; Ishihara T; Esato K; Hamano K; Matsuzaki M. 2005. Regression of abdominal aortic aneurysm by inhibition of c-Jun N-terminal kinase. Nat Med 11(12):1330-8. [PubMed: 16311603]  [MGI Ref ID J:104132]

Young CG; Knight CA; Vickers KC; Westbrook D; Madamanchi NR; Runge MS; Ischiropoulos H; Ballinger SW. 2005. Differential effects of exercise on aortic mitochondria. Am J Physiol Heart Circ Physiol 288(4):H1683-9. [PubMed: 15550530]  [MGI Ref ID J:97385]

Yu H; Zhang W; Yancey PG; Koury MJ; Zhang Y; Fazio S; Linton MF. 2006. Macrophage apolipoprotein E reduces atherosclerosis and prevents premature death in apolipoprotein E and scavenger receptor-class BI double-knockout mice. Arterioscler Thromb Vasc Biol 26(1):150-6. [PubMed: 16269665]  [MGI Ref ID J:127962]

Yu KC; David C; Kadambi S; Stahl A; Hirata K; Ishida T; Quertermous T; Cooper AD; Choi SY. 2004. Endothelial lipase is synthesized by hepatic and aorta endothelial cells and its expression is altered in apoE-deficient mice. J Lipid Res 45(9):1614-23. [PubMed: 15175355]  [MGI Ref ID J:93268]

Yu KC; Jiang Y; Chen W; Cooper AD. 2000. Rapid initial removal of chylomicron remnants by the mouse liver does not require hepatically localized apolipoprotein E J Lipid Res 41(11):1715-27. [PubMed: 11060341]  [MGI Ref ID J:65695]

Yuan Z; Miyoshi T; Bao Y; Sheehan JP; Matsumoto AH; Shi W. 2009. Microarray analysis of gene expression in mouse aorta reveals role of the calcium signaling pathway in control of atherosclerosis susceptibility. Am J Physiol Heart Circ Physiol 296(5):H1336-43. [PubMed: 19304945]  [MGI Ref ID J:150880]

Yuan Z; Pei H; Roberts DJ; Zhang Z; Rowlan JS; Matsumoto AH; Shi W. 2009. Quantitative trait locus analysis of neointimal formation in an intercross between C57BL/6 and C3H/HeJ apolipoprotein E-deficient mice. Circ Cardiovasc Genet 2(3):220-228. [PubMed: 19718279]  [MGI Ref ID J:153521]

Yuan Z; Su Z; Miyoshi T; Rowlan JS; Shi W. 2008. Quantitative trait locus analysis of circulating adhesion molecules in hyperlipidemic apolipoprotein E-deficient mice. Mol Genet Genomics 280(5):375-83. [PubMed: 18704499]  [MGI Ref ID J:153398]

Zaina S; Pettersson L; Ahren B; Branen L; Hassan AB; Lindholm M; Mattsson R; Thyberg J; Nilsson J. 2002. Insulin-like growth factor II plays a central role in atherosclerosis in a mouse model. J Biol Chem 277(6):4505-11. [PubMed: 11726660]  [MGI Ref ID J:74530]

Zernecke A; Bot I; Djalali-Talab Y; Shagdarsuren E; Bidzhekov K; Meiler S; Krohn R; Schober A; Sperandio M; Soehnlein O; Bornemann J; Tacke F; Biessen EA; Weber C. 2008. Protective role of CXC receptor 4/CXC ligand 12 unveils the importance of neutrophils in atherosclerosis. Circ Res 102(2):209-17. [PubMed: 17991882]  [MGI Ref ID J:145593]

Zernecke A; Liehn EA; Fraemohs L; von Hundelshausen P; Koenen RR; Corada M; Dejana E; Weber C. 2006. Importance of junctional adhesion molecule-A for neointimal lesion formation and infiltration in atherosclerosis-prone mice. Arterioscler Thromb Vasc Biol 26(2):e10-3. [PubMed: 16306427]  [MGI Ref ID J:127969]

Zernecke A; Liehn EA; Gao JL; Kuziel WA; Murphy PM; Weber C. 2006. Deficiency in CCR5 but not CCR1 protects against neointima formation in atherosclerosis-prone mice: involvement of IL-10. Blood 107(11):4240-3. [PubMed: 16467202]  [MGI Ref ID J:128843]

Zernecke A; Schober A; Bot I; von Hundelshausen P; Liehn EA; Mopps B; Mericskay M; Gierschik P; Biessen EA; Weber C. 2005. SDF-1alpha/CXCR4 axis is instrumental in neointimal hyperplasia and recruitment of smooth muscle progenitor cells. Circ Res 96(7):784-91. [PubMed: 15761195]  [MGI Ref ID J:137758]

Zhang L; Peppel K; Sivashanmugam P; Orman ES; Brian L; Exum ST; Freedman NJ. 2007. Expression of tumor necrosis factor receptor-1 in arterial wall cells promotes atherosclerosis. Arterioscler Thromb Vasc Biol 27(5):1087-94. [PubMed: 17442899]  [MGI Ref ID J:128059]

Zhang S; Picard MH; Vasile E; Zhu Y; Raffai RL; Weisgraber KH; Krieger M. 2005. Diet-induced occlusive coronary atherosclerosis, myocardial infarction, cardiac dysfunction, and premature death in scavenger receptor class B type I-deficient, hypomorphic apolipoprotein ER61 mice. Circulation 111(25):3457-64. [PubMed: 15967843]  [MGI Ref ID J:114611]

Zhang SH; Reddick RL; Burkey B; Maeda N. 1994. Diet-induced atherosclerosis in mice heterozygous and homozygous for apolipoprotein E gene disruption. J Clin Invest 94(3):937-45. [PubMed: 8083379]  [MGI Ref ID J:20459]

Zhang SH; Reddick RL; Piedrahita JA; Maeda N. 1992. Spontaneous hypercholesterolemia and arterial lesions in mice lacking apolipoprotein E. Science 258(5081):468-71. [PubMed: 1411543]  [MGI Ref ID J:16573]

Zhang W; Yancey PG; Su YR; Babaev VR; Zhang Y; Fazio S; Linton MF. 2003. Inactivation of macrophage scavenger receptor class B type I promotes atherosclerotic lesion development in apolipoprotein E-deficient mice. Circulation 108(18):2258-63. [PubMed: 14581413]  [MGI Ref ID J:103014]

Zhang WJ; Bird KE; McMillen TS; LeBoeuf RC; Hagen TM; Frei B. 2008. Dietary alpha-lipoic acid supplementation inhibits atherosclerotic lesion development in apolipoprotein E-deficient and apolipoprotein E/low-density lipoprotein receptor-deficient mice. Circulation 117(3):421-8. [PubMed: 18158360]  [MGI Ref ID J:145089]

Zhao L; Pratico D; Rader DJ; Funk CD. 2005. 12/15-Lipoxygenase gene disruption and vitamin E administration diminish atherosclerosis and oxidative stress in apolipoprotein E deficient mice through a final common pathway. Prostaglandins Other Lipid Mediat 78(1-4):185-93. [PubMed: 16303615]  [MGI Ref ID J:112785]

Zhou C; King N; Chen KY; Breslow JL. 2009. Activation of pregnane X receptor induces hypercholesterolemia in wild-type and accelerates atherosclerosis in apolipoprotein E deficient mice. J Lipid Res :. [PubMed: 19436068]  [MGI Ref ID J:154141]

Zhou J; Lhotak S; Hilditch BA; Austin RC. 2005. Activation of the unfolded protein response occurs at all stages of atherosclerotic lesion development in apolipoprotein E-deficient mice. Circulation 111(14):1814-21. [PubMed: 15809369]  [MGI Ref ID J:109687]

Zhou X; Hansson GK. 1999. Detection of B cells and proinflammatory cytokines in atherosclerotic plaques of hypercholesterolaemic apolipoprotein E knockout mice. Scand J Immunol 50(1):25-30. [PubMed: 10404048]  [MGI Ref ID J:56605]

Zhou X; Paulsson G; Stemme S; Hansson GK. 1998. Hypercholesterolemia is associated with a T helper (Th) 1/Th2 switch of the autoimmune response in atherosclerotic apo E-knockout mice. J Clin Invest 101(8):1717-25. [PubMed: 9541503]  [MGI Ref ID J:47027]

Zhou X; Robertson AK; Rudling M; Parini P; Hansson GK. 2005. Lesion development and response to immunization reveal a complex role for CD4 in atherosclerosis. Circ Res 96(4):427-34. [PubMed: 15662027]  [MGI Ref ID J:106869]

Zhou X; Stemme S; Hansson GK. 1996. Evidence for a local immune response in atherosclerosis. CD4+ T cells infiltrate lesions of apolipoprotein-E-deficient mice [see comments] Am J Pathol 149(2):359-66. [PubMed: 8701976]  [MGI Ref ID J:34435]

Zhou Y; Cheshire A; Howell LA; Ryan DH; Harris RB. 1999. Neuroautoantibody immunoreactivity in relation to aging and stress in apolipoprotein E-deficient mice. Brain Res Bull 49(3):173-9. [PubMed: 10435780]  [MGI Ref ID J:110915]

Zhu B; Kuhel DG; Witte DP; Hui DY. 2000. Apolipoprotein E inhibits neointimal hyperplasia after arterial injury in mice Am J Pathol 157(6):1839-48. [PubMed: 11106557]  [MGI Ref ID J:66130]

d'Uscio LV; Baker TA; Mantilla CB; Smith L; Weiler D; Sieck GC; Katusic ZS. 2001. Mechanism of endothelial dysfunction in apolipoprotein E-deficient mice. Arterioscler Thromb Vasc Biol 21(6):1017-22. [PubMed: 11397713]  [MGI Ref ID J:103189]

d'Uscio LV; Katusic ZS. 2006. Increased vascular biosynthesis of tetrahydrobiopterin in apolipoprotein E-deficient mice. Am J Physiol Heart Circ Physiol 290(6):H2466-71. [PubMed: 16428344]  [MGI Ref ID J:111845]

d'Uscio LV; Smith LA; Katusic ZS. 2001. Hypercholesterolemia impairs endothelium-dependent relaxations in common carotid arteries of apolipoprotein e-deficient mice. Stroke 32(11):2658-64. [PubMed: 11692031]  [MGI Ref ID J:104001]

van Haperen R; de Waard M; van Deel E; Mees B; Kutryk M; van Aken T; Hamming J; Grosveld F; Duncker DJ; de Crom R. 2002. Reduction of blood pressure, plasma cholesterol, and atherosclerosis by elevated endothelial nitric oxide. J Biol Chem 277(50):48803-7. [PubMed: 12364322]  [MGI Ref ID J:80701]

van Meer P; Pfankuch T; Raber J. 2007. Reduced histamine levels and H3 receptor antagonist-induced histamine release in the amygdala of Apoe-/- mice. J Neurochem 103(1):124-30. [PubMed: 17573822]  [MGI Ref ID J:128042]

von Dehn G; von Dehn O; Volker W; Langer C; Weinbauer GF; Behre HM; Nieschlag E; Assmann G; von Eckardstein A. 2001. Atherosclerosis in apolipoprotein E-deficient mice is decreased by the suppression of endogenous sex hormones. Horm Metab Res 33(2):110-4. [PubMed: 11294492]  [MGI Ref ID J:68906]

Health & husbandry

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Room Number           FGB29

Colony Maintenance

Breeding & HusbandryWhen maintaining a live colony, these mice can be bred as homozygotes.
Mating SystemHeterozygote x Heterozygote         (Female x Male)   04-FEB-09
Diet Information LabDiet® 5K52/5K67

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Pricing for USA, Canada and Mexico shipping destinations View International pricing
Weeks of AgePrice (US dollars $)GenderGenotypes Provided
Individual Mouse $243.50Female or MaleHeterozygous for Apoetm1Unc
Pairs /Price (US dollars $)Pair Genotype
$487.00Heterozygous for Apoetm1Unc x Heterozygous for Apoetm1Unc

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Pricing for International shipping destinations View USA Canada and Mexico pricing
Weeks of AgePrice (US dollars $)GenderGenotypes Provided
Individual Mouse $316.60Female or MaleHeterozygous for Apoetm1Unc
Pairs /Price (US dollars $)Pair Genotype
$633.10Heterozygous for Apoetm1Unc x Heterozygous for Apoetm1Unc

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Standard SupplyRepository-Live. A collection of over 1000 strains maintained as live colonies. Individual colonies are sized to meet current customer demand. Delivery for orders of 10 mice or less ranges on average from one to eight weeks; mice are generally shipped between four to six weeks of age with a maximum shipping age of approximately nine weeks. Colony sizes do not generally support stringent age specifications for large volumes of mice; however custom orders and larger quantities of mice are easily arranged. Estimated ship dates for all orders provided within two business days following order placement.
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   000671 DBA/2J
 
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