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Description
Strain Information
Former Names B6.Cg-Spp1tm1Blh/J (Changed: 05-NOV-07 ) Type Congenic; Mutant Strain; Targeted Mutation; Additional information on Genetically Engineered and Mutant Mice. Visit our online Nomenclature tutorial. Additional information on Congenic nomenclature. Mating System Homozygote x Homozygote (Female x Male) 01-MAR-06 Species laboratory mouse Generation N10+N2F5 (11-MAY-11)
Generation DefinitionsDonating Investigator Lucy Liaw, Maine Medical Center Research Institute Description
Mice that are homozygous for the targeted mutation are viable, fertile, normal in size and do not display any gross physical or behavioral abnormalities. No gene product (mRNA) is detected by RT-PCR analysis of embryonic fibroblasts and kidney. Immunohistochemical analysis of kidney and bone tissue also fails to detect gene product (protein). Homozygotes exhibit disorganized ultrastructural wound matrix remodeling and defective macrophage infiltration and accumulation at sites of injury and infection. Experimentally induced hyperoxaluria results in renal tubule deposition of calcium oxalate crystals. Accelerated ectopic calcification mineralization in soft tissues occurs after subcutaneous implantation of glutaraldehyde-fixed aortic valve tissue. Mutant macrophage response to mycobacteria infection and pulmonary granulomatous response and inflammation are impaired. According to a recent publication (Hsieh et al 2006 Cancer Res 2006 66:7119-27), mutant mice treated with a skin chemical carcinogenesis protocol show a marked decrease both in tumor/papilloma incidence and multiplicity compared with wildtype. This mutant mouse strain may be useful in studies of tissue remodeling, wound repair, fibrosis and granulomatous diseases.All of the characterization of this mutant was performed while the mutant allele was on a mixed 129S6, Black Swiss background. The phenotype of the donated mutant, which is on a congenic C57BL/6 background, may vary.
Development
A targeting vector containing neomycin resistance and herpes simplex virus thymidine kinase genes was used to disrupt exons 4 through 7 of the targeted gene. The construct was electroporated into 129S6/SvEvTac derived TL-1 embryonic stem (ES) cells. Correctly targeted ES cells were injected into C57BL/6 blastocysts. The resulting chimeric animals were crossed to outbred Black Swiss, maintained on the mixed Black Swiss;129S6 background, and then backcrossed to C57BL/6 for 10 generations (March 2003; see SNP note below).A 32 SNP (single nucleotide polymorphism) panel analysis, with 27 markers covering all 19 chromosomes and the X chromosome, as well as 5 markers that distinguish between the C57BL/6J and C57BL/6N substrains, was performed on the rederived living colony at The Jackson Laboratory Repository. While the 27 markers throughout the genome suggested a C57BL/6 genetic background, 1 of 5 markers that determine C57BL/6J from C57BL/6N were found to be segregating. These data suggest the mice sent to The Jackson Laboratory Repository were on a mixed C57BL/6J ; C57BL/6N genetic background.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
Related Strains
Parkinson's Disease Models
View Parkinson's Disease Models (99 strains)
Additional Web Information
Genetic Quality Control Annual Report
Visit the Parkinson's Disease Resource site for helpful information on Parkinson's and research resources.
Phenotype
Phenotype Information
assigned by genotype
Spp1tm1Blh/Spp1tm1Blh
B6.129S6(Cg)-Spp1tm1Blh/J
- reproductive system phenotype
- *normal* reproductive system phenotype
- despite strong Spp1+ mRNA expression in wild-type testis cords and protein localization in the cytoplasm of Sertoli cells, testes from E13.5 homozygotes show no differences in the number or distribution of Sertoli, Leydig, or germ cells relative to wild-type testes (MGI Ref ID J:99574)
- hematopoietic system phenotype
- abnormal hematopoietic system physiology
- decreased hematocrit
- decreased hemoglobin content
Spp1tm1Blh/Spp1tm1Blh
B6.129S6-Spp1tm1Blh
- nervous system phenotype
- abnormal microglial cell morphology
- MPTP-treated mice exhibit decreased microglial cells with longer processes compared with similarly treated wild-type mice (MGI Ref ID J:118432)
- abnormal striatum morphology
- tyrosine hydroxylase (TH) positive nerve fibers in the striatum are decreased to a lesser extent in MPTP-treated homozygotes than in MPTP-treated wildtype mice (MGI Ref ID J:118432)
- abnormal substantia nigra morphology
- MPTP-treated homozygotes exhibit an increase in the number of microglial cells, however, MPTP-treated wildtype mice exhibited a greater increase (MGI Ref ID J:118432)
- numbers of GFAP-positive astrocytes increased in the MPTP-treated wildtype mice, but not in MPTP-treated homozygotes or sham-treated wildtype mice (MGI Ref ID J:118432)
- astrocytic processes are longer in MPTP-treated homozygotes than in both MPTP-treated wildtype and sham-treated wildtype mice (MGI Ref ID J:118432)
- decreased susceptibility to dopaminergic neuron neurotoxicity
- neuronal cell death in MPTP-treated homozygotes is comparable to sham-treated wildtype and significantly less than MPTP-treated wildtype, suggesting a protective effect (MGI Ref ID J:118432)
- increased neuron number
- MPTP-treated mice exhibit increased neuron and TH+ fiber survival compared to in similarly treated wild-type mice (MGI Ref ID J:118432)
- immune system phenotype
- abnormal microglial cell morphology
- MPTP-treated mice exhibit decreased microglial cells with longer processes compared with similarly treated wild-type mice (MGI Ref ID J:118432)
- decreased susceptibility to experimental autoimmune uveoretinitis
- mice exhibit decreased incidence of experimental autoimmune uveoretinitis with fewer infiltrating inflammatory cells in the vitreous, decreased granulomas, and reduced lymphocyte proliferation compared with similarly treated wild-type mice (MGI Ref ID J:116272)
- granulomatous inflammation
- mice exhibit decreased granulomas in a model of experimental autoimmune uveoretinitis compared with similarly treated wild-type mice (MGI Ref ID J:116272)
- hematopoietic system phenotype
- abnormal microglial cell morphology
- MPTP-treated mice exhibit decreased microglial cells with longer processes compared with similarly treated wild-type mice (MGI Ref ID J:118432)
- homeostasis/metabolism phenotype
- decreased physiological sensitivity to xenobiotic
- MPTP-treated mice exhibit increased neuron and TH+ fiber survival and decreased microglial cells with longer processes compared with similarly treated wild-type mice (MGI Ref ID J:118432)
- decreased susceptibility to dopaminergic neuron neurotoxicity
- neuronal cell death in MPTP-treated homozygotes is comparable to sham-treated wildtype and significantly less than MPTP-treated wildtype, suggesting a protective effect (MGI Ref ID J:118432)
- cellular phenotype
- decreased susceptibility to dopaminergic neuron neurotoxicity
- neuronal cell death in MPTP-treated homozygotes is comparable to sham-treated wildtype and significantly less than MPTP-treated wildtype, suggesting a protective effect (MGI Ref ID J:118432)
The following phenotype information may relate to a genetic background differing from this JAX® Mice strain.
Spp1tm1Blh/Spp1+
BKSW.129S6-Spp1tm1Blh
- immune system phenotype
- abnormal immune system physiology
- the foreign body response provoked by glutaraldehyde-fixed aortic valve leaflets is diminished in quality with a four- to five-fold increase calcification of the leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
- other phenotype
- calcinosis
- the foreign body response provoked by glutaraldehyde-fixed aortic valve leaflets is diminished in quality with a four- to five-fold increase calcification of the leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
Spp1tm1Blh/Spp1+
involves: 129S6/SvEvTac * Black Swiss
- immune system phenotype
- abnormal leukocyte migration
- leukocytes exhibit decreased basal and MCP-1-dependent migration compared with similarly treated wild-type cells (MGI Ref ID J:86531)
- cellular phenotype
- abnormal leukocyte migration
- leukocytes exhibit decreased basal and MCP-1-dependent migration compared with similarly treated wild-type cells (MGI Ref ID J:86531)
Spp1tm1Blh/Spp1tm1Blh
involves: 129S6/SvEvTac * Black Swiss
- mortality/aging
- *normal* mortality/aging
- under normal conditions, homozygotes are viable and fertile, with no apparent defects in growth, external morphology or behavior (MGI Ref ID J:46863)
- importantly, unwounded skin from homozygotes displays normal tissue architecture and cell organization in the subepithelial, middermal, and deep dermal regions; differences in dermal organization become significant only in the context of the healing process (MGI Ref ID J:46863)
- immune system phenotype
- abnormal chemokine level
- when fed a high-fat diet, plasma levels of MCP-1 (Ccl2) and PAI-1 (Serpine1) are decreased compared to in similarly treated wild-type mice (MGI Ref ID J:127389)
- abnormal leukocyte physiology
- leukocytes from peritoneal exudates of Ang-II-stimulated mice exhibit decreased viability compared with cells from similarly treated wild-type mice (MGI Ref ID J:86531)
- abnormal leukocyte migration
- leukocytes exhibit decreased basal and absent MCP-1-dependent migration compared with similarly treated wild-type and heterozygous cells (MGI Ref ID J:86531)
- abnormal macrophage physiology
- microphages are hypomotile with reduced basal motility and absent MCP-1-stimulated motility unlike wild-type cells (MGI Ref ID J:127389)
- exogenous Spp1 only partially rescues macrophage motility (MGI Ref ID J:127389)
- migration of macrophages from obese mice towards stromal vascular cells is decreased compared with wild-type cells (MGI Ref ID J:127389)
- abnormal response to infection
- following exposure to Schistosoma mansoni eggs, pulmonary granuloma lesions formation is delayed, granuloma size is reduced at early time points but increased at later time points, and clearance is delayed compared to in similarly treated wild-type mice (MGI Ref ID J:103013)
- at day 75 of S. mansoni infection, granulomas are composed of mononuclear cells unlike wild-type granulomas with epithelioid morphology (MGI Ref ID J:103013)
- S. mansoni egg-exposed mice exhibit reduced giant cells in granulomas until day 75 when giant cell formation is increased compared to in similarly treated wild-type mice (MGI Ref ID J:103013)
- S. mansoni egg-exposed mice exhibit granulomas with few or no macrophages unlike in similarly treated wild-type mice (MGI Ref ID J:103013)
- however, T cell accumulation in S. mansoni egg granulomas is normal (MGI Ref ID J:103013)
- decreased circulating interleukin-6 level
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- decreased leukocyte cell number
- decreased macrophage cell number
- mice fed a high-fat diet exhibit reduced accumulation of macrophages in adipose tissue compared with similarly treated wild-type mice (MGI Ref ID J:127389)
- granulomatous inflammation
- overall greater burden of granulomas after infection than in controls, 3.1% of liver tissue compared to 1.1% (MGI Ref ID J:140014)
- increased lymphocyte cell number (MGI Ref ID J:103050)
- homeostasis/metabolism phenotype
- *normal* homeostasis/metabolism phenotype
- mice exhibit normal serum and urine biochemistry (MGI Ref ID J:103140)
- abnormal chemokine level
- when fed a high-fat diet, plasma levels of MCP-1 (Ccl2) and PAI-1 (Serpine1) are decreased compared to in similarly treated wild-type mice (MGI Ref ID J:127389)
- abnormal wound healing
- at 2 weeks after dermal incisional wounding, homozygotes exhibit reduced debridement throughout the wound site, esp. in the subepithelial dermis (MGI Ref ID J:46863)
- in resolving wounds, the reforming matrix appears to be less organized in both the subepithelial and middermal regions (MGI Ref ID J:46863)
- in the subepithelial and middermal zones, the organization of collagen fibrils and fibers is less distinct (MGI Ref ID J:46863)
- in the deep reticular dermis, the collagen fibril diameter is significantly smaller; fibrils remain small, with a homogeneous distribution at all wound levels (MGI Ref ID J:46863)
- notably, homozygotes show no significant differences in tensile strength of healing incisional wounds relative to wild-type mice (MGI Ref ID J:46863)
- abnormal vascular wound healing
- following carotid artery ligation, mice exhibit a 10-fold decrease leukocyte infiltration, decreased neointimal formation, and greater constrictive remodeling resulting in normal lumen area but decreased medial area compared with similarly treated wild-type mice (MGI Ref ID J:103050)
- however, cell proliferation and apoptosis during blood vessel healing is normal at 14 days (MGI Ref ID J:103050)
- altered response to myocardial infarction
- following myocardial infarction, mice exhibit increased left ventricular mid-papillary circumference, lung weight, and left ventricle volume to heart weight ratio with a greater rightward shift in left ventricle pressure-volume relationship and decreases in chamber stiffness constant, myocyte length, and collagen content compared with similarly treated wild-type mice (MGI Ref ID J:115399)
- however, mice exhibit normal infarct size, heart weight, number of apoptotic myocytes, and survival (MGI Ref ID J:115399)
- crystalluria
- 4 weeks following hyperoxaluria induction with 1% ethylene glycol, mice exhibit CaOx monohydrate crystalluria and retention in renal tubes unlike treated wild-type mice (MGI Ref ID J:103140)
- decreased circulating glucose level
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- decreased circulating insulin level
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- decreased circulating interleukin-6 level
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- decreased circulating triglyceride level
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- improved glucose tolerance
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- increased insulin sensitivity
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- increased physiological sensitivity to xenobiotic
- bleomycin-treated mice exhibit an increase in the number and size of cystic epithelial lined air spaces within fibrotic areas of the lung compared to in similarly treated wild-type mice (MGI Ref ID J:108144)
- increased respiratory quotient
- when fed a high-fat diet, mice exhibit a modest increase in respiratory quotient during the 12-hour light cycle compared with similarly treated wild-type mice (MGI Ref ID J:127389)
- however, mice fed a high-fat diet exhibit a normal respiratory quotient when analyzed over a 24 hour period (MGI Ref ID J:127389)
- cardiovascular system phenotype
- abnormal blood flow velocity
- blood flow at similar heart rates is decreased compared to in wild-type mice (MGI Ref ID J:103050)
- abnormal blood vessel morphology
- decreased susceptibility to atherosclerosis
- abnormal blood vessel physiology
- vascular tone and compliance are increased compared to in wild-type mice (MGI Ref ID J:103050)
- abnormal vascular wound healing
- following carotid artery ligation, mice exhibit a 10-fold decrease leukocyte infiltration, decreased neointimal formation, and greater constrictive remodeling resulting in normal lumen area but decreased medial area compared with similarly treated wild-type mice (MGI Ref ID J:103050)
- however, cell proliferation and apoptosis during blood vessel healing is normal at 14 days (MGI Ref ID J:103050)
- abnormal vasodilation
- blood vessels dilate rapidly at lower pressures than similarly treated wild-type vessels (MGI Ref ID J:103050)
- altered response to myocardial infarction
- following myocardial infarction, mice exhibit increased left ventricular mid-papillary circumference, lung weight, and left ventricle volume to heart weight ratio with a greater rightward shift in left ventricle pressure-volume relationship and decreases in chamber stiffness constant, myocyte length, and collagen content compared with similarly treated wild-type mice (MGI Ref ID J:115399)
- however, mice exhibit normal infarct size, heart weight, number of apoptotic myocytes, and survival (MGI Ref ID J:115399)
- decreased systemic arterial blood pressure (MGI Ref ID J:103050)
- decreased systemic arterial systolic blood pressure (MGI Ref ID J:103050)
- increased heart rate (MGI Ref ID J:103050)
- renal/urinary system phenotype
- *normal* renal/urinary system phenotype
- mice exhibit normal urine biochemistry (MGI Ref ID J:103140)
- crystalluria
- 4 weeks following hyperoxaluria induction with 1% ethylene glycol, mice exhibit CaOx monohydrate crystalluria and retention in renal tubes unlike treated wild-type mice (MGI Ref ID J:103140)
- respiratory system phenotype
- increased lung weight
- following myocardial infarction (MGI Ref ID J:115399)
- lung cysts
- bleomycin-treated mice exhibit an increase in the number and size of cystic epithelial lined air spaces within fibrotic areas of the lung compared to in similarly treated wild-type mice (MGI Ref ID J:108144)
- growth/size phenotype
- decreased lean body mass
- compared to in wild-type mice when fed a high-fat diet (MGI Ref ID J:127389)
- hematopoietic system phenotype
- decreased leukocyte cell number
- decreased macrophage cell number
- mice fed a high-fat diet exhibit reduced accumulation of macrophages in adipose tissue compared with similarly treated wild-type mice (MGI Ref ID J:127389)
- increased lymphocyte cell number (MGI Ref ID J:103050)
- muscle phenotype
- abnormal vasodilation
- blood vessels dilate rapidly at lower pressures than similarly treated wild-type vessels (MGI Ref ID J:103050)
- cellular phenotype
- abnormal leukocyte migration
- leukocytes exhibit decreased basal and absent MCP-1-dependent migration compared with similarly treated wild-type and heterozygous cells (MGI Ref ID J:86531)
Spp1tm1Blh/Spp1tm1Blh
involves: 129S6/SvEvTac * C57BL/6
- immune system phenotype
- abnormal immune system physiology
- 75% less injected wild-type dendritic cells enter the axillary and inguinal lymph nodes (MGI Ref ID J:119298)
- decreased dendritic cell number
- mice sensitized with TNCB and challenged hapten exhibit reduced numbers of CD11c+FITC+ cells in the skin draining lymph nodes compared with similarly treated wild-type mice (MGI Ref ID J:119298)
- homeostasis/metabolism phenotype
- decreased physiological sensitivity to xenobiotic
- mice sensitized with TNCB and challenged hapten exhibit reduced ear swelling and reduced numbers of CD11c+FITC+ cells in the skin draining lymph nodes compared with similarly treated wild-type mice (MGI Ref ID J:119298)
- hematopoietic system phenotype
- decreased dendritic cell number
- mice sensitized with TNCB and challenged hapten exhibit reduced numbers of CD11c+FITC+ cells in the skin draining lymph nodes compared with similarly treated wild-type mice (MGI Ref ID J:119298)
Spp1tm1Blh/Spp1tm1Blh
BKSW.129S6-Spp1tm1Blh
- immune system phenotype
- abnormal immune system physiology
- the foreign body response provoked by glutaraldehyde-fixed aortic valve leaflets is diminished in quality with a 50% to 25% reduction in macrophage recruitment, a four- to five-fold increase calcification of the leaflet, and acidification of the leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
- impaired macrophage chemotaxis
- mice exhibit a 50% to 25% reduction in macrophage recruitment to a transplanted glutaraldehyde-fixed aortic valve leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
- other phenotype
- calcinosis
- the foreign body response provoked by glutaraldehyde-fixed aortic valve leaflets is diminished in quality with a four- to five-fold increase calcification of the leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
- cellular phenotype
- impaired macrophage chemotaxis
- mice exhibit a 50% to 25% reduction in macrophage recruitment to a transplanted glutaraldehyde-fixed aortic valve leaflet compared to in similarly treated wild-type mice (MGI Ref ID J:113585)
Spp1tm1Blh/Spp1tm1Blh
involves: 129S6/SvEvTac
- skeleton phenotype
- abnormal bone mineralization
- crystallinity in the bones of younger mice is increased compared to in wild-type mice (MGI Ref ID J:81625)
- increased bone mineral density
- at 16 weeks, the ratio of mineral to matrix is increased in the cortical center and area of cortical bone adjacent to the endosteum compared to in wild-type mice (MGI Ref ID J:81625)
This mouse can be used to support research in many areas including:
Spp1tm1Blh relatedNeurobiology Research
Parkinson's Disease
resistance to MPTP
Immunology and Inflammation Research
Immunodeficiency Associated with Other Defects
Inflammation
Internal/Organ Research
Wound Healing
Genes & Alleles
Gene & Allele Information provided by MGI
| Allele Symbol | Spp1tm1Blh | ||
|---|---|---|---|
| Allele Name | targeted mutation 1, Brigid L Hogan | ||
| Allele Type | Targeted (knock-out) | ||
| Common Name(s) | Eta-1; OPN-KO; OPN-; Opn-; eta1; | ||
| Mutation Made By | Lucy Liaw, Maine Medical Center Research Institute | ||
| Strain of Origin | 129S6/SvEvTac | ||
| ES Cell Line Name | TL1/TL-1 | ||
| ES Cell Line Strain | 129S6/SvEvTac | ||
| Gene Symbol and Name | Spp1, secreted phosphoprotein 1 | ||
| Chromosome | 5 | ||
| Gene Common Name(s) | 2ar; 44kDa bone phosphoprotein; AA960535; AI790405; Apl-1; BNSP; BSPI; ETA-1; Eta; OP; OPN; OSP; Opn; Opnl; Ric; Spp-1; activation protein lymphocyte 1; bone sialoprotein 1; early T lymphocyte activation; expressed sequence AA960535; expressed sequence AI790405; minopontin; osteopontin; osteopontin-like protein; rickettsia tsutsugamushi resistance; | ||
| Molecular Note | A PGK neomycin resistance cassette replaced exons 4-7 of the Spp1 gene. No Spp1 transcript was detected by RT-PCR in embryonic fibroblasts or adult kidney from homozygous mutant animals. Spp1 transcript was not detected in homozygous mutant animals by in situ hybridization. Immunohistochemistry studies of adult kidney and bone did not detect protein in homozygous mutant mice. [MGI Ref ID J:46863] | ||
Genotyping
Genotyping Information
Genotyping Protocols
Spp1tm1Blh, Standard PCR
Helpful Links
Genotyping resources and troubleshooting
References
References provided by MGI
Selected Reference(s)
Liaw L; Birk DE; Ballas CB; Whitsitt JS; Davidson JM; Hogan BL. 1998. Altered wound healing in mice lacking a functional osteopontin gene (spp1). J Clin Invest 101(7):1468-78. [PubMed: 9525990] [MGI Ref ID J:46863]
Additional References
Speer MY; McKee MD; Guldberg RE; Liaw L; Yang HY; Tung E; Karsenty G; Giachelli CM. 2002. Inactivation of the osteopontin gene enhances vascular calcification of matrix Gla protein-deficient mice: evidence for osteopontin as an inducible inhibitor of vascular calcification in vivo. J Exp Med 196(8):1047-55. [PubMed: 12391016] [MGI Ref ID J:79746]
Spp1tm1Blh relatedAbel B; Freigang S; Bachmann MF; Boschert U; Kopf M. 2005. Osteopontin is not required for the development of Th1 responses and viral immunity. J Immunol 175(9):6006-13. [PubMed: 16237095] [MGI Ref ID J:119351]
Abel B; Kurrer M; Shamshiev A; Marty RR; Eriksson U; Gunthert U; Kopf M. 2006. The osteopontin - CD44 pathway is superfluous for the development of autoimmune myocarditis. Eur J Immunol 36(2):494-9. [PubMed: 16402410] [MGI Ref ID J:113855]
Bazigou E; Xie S; Chen C; Weston A; Miura N; Sorokin L; Adams R; Muro AF; Sheppard D; Makinen T. 2009. Integrin-alpha9 is required for fibronectin matrix assembly during lymphatic valve morphogenesis. Dev Cell 17(2):175-86. [PubMed: 19686679] [MGI Ref ID J:152968]
Berman JS; Serlin D; Li X; Whitley G; Hayes J; Rishikof DC; Ricupero DA; Liaw L; Goetschkes M; O'Regan AW. 2004. Altered bleomycin-induced lung fibrosis in osteopontin-deficient mice. Am J Physiol Lung Cell Mol Physiol 286(6):L1311-8. [PubMed: 14977630] [MGI Ref ID J:108144]
Boskey AL; Spevak L; Paschalis E; Doty SB; McKee MD. 2002. Osteopontin deficiency increases mineral content and mineral crystallinity in mouse bone. Calcif Tissue Int 71(2):145-54. [PubMed: 12073157] [MGI Ref ID J:81625]
Bruemmer D; Collins AR; Noh G; Wang W; Territo M; Arias-Magallona S; Fishbein MC; Blaschke F; Kintscher U; Graf K; Law RE; Hsueh WA. 2003. Angiotensin II-accelerated atherosclerosis and aneurysm formation is attenuated in osteopontin-deficient mice. J Clin Invest 112(9):1318-31. [PubMed: 14597759] [MGI Ref ID J:86531]
Chakraborty G; Jain S; Patil TV; Kundu GC. 2008. Down-Regulation of Osteopontin Attenuates Breast Tumor Progression in vivo. J Cell Mol Med :. [PubMed: 18266970] [MGI Ref ID J:142483]
Chapman J; Miles PD; Ofrecio JM; Neels JG; Yu JG; Resnik JL; Wilkes J; Talukdar S; Thapar D; Johnson K; Sears DD. 2010. Osteopontin is required for the early onset of high fat diet-induced insulin resistance in mice. PLoS One 5(11):e13959. [PubMed: 21103061] [MGI Ref ID J:166990]
Duvall CL; Taylor WR; Weiss D; Wojtowicz AM; Guldberg RE. 2007. Impaired angiogenesis, early callus formation, and late stage remodeling in fracture healing of osteopontin-deficient mice. J Bone Miner Res 22(2):286-97. [PubMed: 17087627] [MGI Ref ID J:133152]
Duvall CL; Weiss D; Robinson ST; Alameddine FM; Guldberg RE; Taylor WR. 2008. The role of osteopontin in recovery from hind limb ischemia. Arterioscler Thromb Vasc Biol 28(2):290-5. [PubMed: 18006856] [MGI Ref ID J:159820]
Fickert P; Thueringer A; Moustafa T; Silbert D; Gumhold J; Tsybrovskyy O; Lebofsky M; Jaeschke H; Denk H; Trauner M. 2010. The role of osteopontin and tumor necrosis factor alpha receptor-1 in xenobiotic-induced cholangitis and biliary fibrosis in mice. Lab Invest 90(6):844-52. [PubMed: 20368698] [MGI Ref ID J:160746]
Fujihara S; Yokozeki M; Oba Y; Higashibata Y; Nomura S; Moriyama K. 2006. Function and regulation of osteopontin in response to mechanical stress. J Bone Miner Res 21(6):956-64. [PubMed: 16753026] [MGI Ref ID J:128094]
Goncalves DaSilva A; Liaw L; Yong VW. 2010. Cleavage of osteopontin by matrix metalloproteinase-12 modulates experimental autoimmune encephalomyelitis disease in C57BL/6 mice. Am J Pathol 177(3):1448-58. [PubMed: 20651245] [MGI Ref ID J:163629]
Hikita ST; Vistica BP; Jones HR; Keswani JR; Watson MM; Ericson VR; Ayoub GS; Gery I; Clegg DO. 2006. Osteopontin is proinflammatory in experimental autoimmune uveitis. Invest Ophthalmol Vis Sci 47(10):4435-43. [PubMed: 17003437] [MGI Ref ID J:116272]
Hoshino K; Sasaki I; Sugiyama T; Yano T; Yamazaki C; Yasui T; Kikutani H; Kaisho T. 2010. Critical role of IkappaB Kinase alpha in TLR7/9-induced type I IFN production by conventional dendritic cells. J Immunol 184(7):3341-5. [PubMed: 20200270] [MGI Ref ID J:160080]
Hsieh YH; Juliana MM; Hicks PH; Feng G; Elmets C; Liaw L; Chang PL. 2006. Papilloma development is delayed in osteopontin-null mice: implicating an antiapoptosis role for osteopontin. Cancer Res 66(14):7119-27. [PubMed: 16849558] [MGI Ref ID J:112122]
Ishii T; Ohshima S; Ishida T; Kawase I; Mima T; Tabunoki Y; Kobayashi H; Maeda M; Uede T; Liaw L; Kinoshita N; Saeki Y. 2004. Mice with osteopontin deletion remain predisposed to collagen-induced arthritis. Arthritis Rheum 50(2):669-71. [PubMed: 14872512] [MGI Ref ID J:106166]
Kang JA; Zhou Y; Weis TL; Liu H; Ulaszek J; Satgurunathan N; Zhou L; van Besien K; Crispino J; Verma A; Low PS; Wickrema A. 2008. Osteopontin regulates actin cytoskeleton and contributes to cell proliferation in primary erythroblasts. J Biol Chem 283(11):6997-7006. [PubMed: 18174176] [MGI Ref ID J:133795]
Kiefer FW; Neschen S; Pfau B; Legerer B; Neuhofer A; Kahle M; Hrabe de Angelis M; Schlederer M; Mair M; Kenner L; Plutzky J; Zeyda M; Stulnig TM. 2011. Osteopontin deficiency protects against obesity-induced hepatic steatosis and attenuates glucose production in mice. Diabetologia :. [PubMed: 21562757] [MGI Ref ID J:172597]
Kilic G; Wang J; Sosa-Pineda B. 2006. Osteopontin is a novel marker of pancreatic ductal tissues and of undifferentiated pancreatic precursors in mice. Dev Dyn 235(6):1659-67. [PubMed: 16518820] [MGI Ref ID J:108608]
Kohan M; Breuer R; Berkman N. 2009. Osteopontin induces airway remodeling and lung fibroblast activation in a murine model of asthma. Am J Respir Cell Mol Biol 41(3):290-6. [PubMed: 19151319] [MGI Ref ID J:163798]
Kokubo T; Ishikawa N; Uchida H; Chasnoff SE; Xie X; Mathew S; Hruska KA; Choi ET. 2009. CKD accelerates development of neointimal hyperplasia in arteriovenous fistulas. J Am Soc Nephrol 20(6):1236-45. [PubMed: 19423694] [MGI Ref ID J:164967]
Lorenzen J; Shah R; Biser A; Staicu SA; Niranjan T; Garcia AM; Gruenwald A; Thomas DB; Shatat IF; Supe K; Woroniecki RP; Susztak K. 2008. The role of osteopontin in the development of albuminuria. J Am Soc Nephrol 19(5):884-90. [PubMed: 18443355] [MGI Ref ID J:150239]
Maetzler W; Berg D; Funke C; Sandmann F; Stunitz H; Maetzler C; Nitsch C. 2010. Progressive secondary neurodegeneration and microcalcification co-occur in osteopontin-deficient mice. Am J Pathol 177(2):829-39. [PubMed: 20522649] [MGI Ref ID J:163413]
Maetzler W; Berg D; Schalamberidze N; Melms A; Schott K; Mueller JC; Liaw L; Gasser T; Nitsch C. 2007. Osteopontin is elevated in Parkinson's disease and its absence leads to reduced neurodegeneration in the MPTP model. Neurobiol Dis 25(3):473-82. [PubMed: 17188882] [MGI Ref ID J:118432]
Mo L; Liaw L; Evan AP; Sommer AJ; Lieske JC; Wu XR. 2007. Renal calcinosis and stone formation in mice lacking osteopontin, Tamm-Horsfall protein, or both. Am J Physiol Renal Physiol 293(6):F1935-43. [PubMed: 17898038] [MGI Ref ID J:127526]
Murugaiyan G; Mittal A; Weiner HL. 2008. Increased osteopontin expression in dendritic cells amplifies IL-17 production by CD4+ T cells in experimental autoimmune encephalomyelitis and in multiple sclerosis. J Immunol 181(11):7480-8. [PubMed: 19017937] [MGI Ref ID J:142205]
Myers DL; Harmon KJ; Lindner V; Liaw L. 2003. Alterations of arterial physiology in osteopontin-null mice. Arterioscler Thromb Vasc Biol 23(6):1021-8. [PubMed: 12714436] [MGI Ref ID J:103050]
Nau GJ; Liaw L; Chupp GL; Berman JS; Hogan BL; Young RA. 1999. Attenuated host resistance against Mycobacterium bovis BCG infection in mice lacking osteopontin. Infect Immun 67(8):4223-30. [PubMed: 10417195] [MGI Ref ID J:140014]
Nomiyama T; Perez-Tilve D; Ogawa D; Gizard F; Zhao Y; Heywood EB; Jones KL; Kawamori R; Cassis LA; Tschop MH; Bruemmer D. 2007. Osteopontin mediates obesity-induced adipose tissue macrophage infiltration and insulin resistance in mice. J Clin Invest 117(10):2877-88. [PubMed: 17823662] [MGI Ref ID J:127389]
O'Regan AW; Hayden JM; Body S; Liaw L; Mulligan N; Goetschkes M; Berman JS. 2001. Abnormal pulmonary granuloma formation in osteopontin-deficient mice. Am J Respir Crit Care Med 164(12):2243-7. [PubMed: 11751194] [MGI Ref ID J:103013]
Okada A; Nomura S; Saeki Y; Higashibata Y; Hamamoto S; Hirose M; Itoh Y; Yasui T; Tozawa K; Kohri K. 2008. Morphological conversion of calcium oxalate crystals into stones is regulated by osteopontin in mouse kidney. J Bone Miner Res 23(10):1629-37. [PubMed: 18505365] [MGI Ref ID J:153414]
Sabo-Attwood T; Ramos-Nino ME; Eugenia-Ariza M; Macpherson MB; Butnor KJ; Vacek PC; McGee SP; Clark JC; Steele C; Mossman BT. 2011. Osteopontin modulates inflammation, mucin production, and gene expression signatures after inhalation of asbestos in a murine model of fibrosis. Am J Pathol 178(5):1975-85. [PubMed: 21514415] [MGI Ref ID J:171594]
Schulz G; Renkl AC; Seier A; Liaw L; Weiss JM. 2008. Regulated osteopontin expression by dendritic cells decisively affects their migratory capacity. J Invest Dermatol 128(10):2541-4. [PubMed: 18449212] [MGI Ref ID J:141700]
Seier AM; Renkl AC; Schulz G; Uebele T; Sindrilaru A; Iben S; Liaw L; Kon S; Uede T; Weiss JM. 2010. Antigen-specific induction of osteopontin contributes to the chronification of allergic contact dermatitis. Am J Pathol 176(1):246-58. [PubMed: 20008129] [MGI Ref ID J:156488]
Simoes DC; Xanthou G; Petrochilou K; Panoutsakopoulou V; Roussos C; Gratziou C. 2009. Osteopontin deficiency protects against airway remodeling and hyperresponsiveness in chronic asthma. Am J Respir Crit Care Med 179(10):894-902. [PubMed: 19234104] [MGI Ref ID J:165088]
Song JJ; Hwang I; Cho KH; Garcia MA; Kim AJ; Wang TH; Lindstrom TM; Lee AT; Nishimura T; Zhao L; Morser J; Nesheim M; Goodman SB; Lee DM; Bridges SL Jr; Gregersen PK; Leung LL; Robinson WH. 2011. Plasma carboxypeptidase B downregulates inflammatory responses in autoimmune arthritis. J Clin Invest 121(9):3517-27. [PubMed: 21804193] [MGI Ref ID J:178261]
Speer MY; Chien YC; Quan M; Yang HY; Vali H; McKee MD; Giachelli CM. 2005. Smooth muscle cells deficient in osteopontin have enhanced susceptibility to calcification in vitro. Cardiovasc Res 66(2):324-33. [PubMed: 15820201] [MGI Ref ID J:162741]
Speer MY; McKee MD; Guldberg RE; Liaw L; Yang HY; Tung E; Karsenty G; Giachelli CM. 2002. Inactivation of the osteopontin gene enhances vascular calcification of matrix Gla protein-deficient mice: evidence for osteopontin as an inducible inhibitor of vascular calcification in vivo. J Exp Med 196(8):1047-55. [PubMed: 12391016] [MGI Ref ID J:79746]
Steitz SA; Speer MY; McKee MD; Liaw L; Almeida M; Yang H; Giachelli CM. 2002. Osteopontin inhibits mineral deposition and promotes regression of ectopic calcification. Am J Pathol 161(6):2035-46. [PubMed: 12466120] [MGI Ref ID J:113585]
Subramanian V; Krishnamurthy P; Singh K; Singh M. 2007. Lack of osteopontin improves cardiac function in streptozotocin-induced diabetic mice. Am J Physiol Heart Circ Physiol 292(1):H673-83. [PubMed: 16980342] [MGI Ref ID J:119943]
Thurner PJ; Chen CG; Ionova-Martin S; Sun L; Harman A; Porter A; Ager JW 3rd; Ritchie RO; Alliston T. 2010. Osteopontin deficiency increases bone fragility but preserves bone mass. Bone 46(6):1564-73. [PubMed: 20171304] [MGI Ref ID J:162044]
Trueblood NA; Xie Z; Communal C; Sam F; Ngoy S; Liaw L; Jenkins AW; Wang J; Sawyer DB; Bing OH; Apstein CS; Colucci WS; Singh K. 2001. Exaggerated left ventricular dilation and reduced collagen deposition after myocardial infarction in mice lacking osteopontin. Circ Res 88(10):1080-7. [PubMed: 11375279] [MGI Ref ID J:115399]
Vetrone SA; Montecino-Rodriguez E; Kudryashova E; Kramerova I; Hoffman EP; Liu SD; Miceli MC; Spencer MJ. 2009. Osteopontin promotes fibrosis in dystrophic mouse muscle by modulating immune cell subsets and intramuscular TGF-beta. J Clin Invest 119(6):1583-94. [PubMed: 19451692] [MGI Ref ID J:150572]
Weiss JM; Renkl AC; Maier CS; Kimmig M; Liaw L; Ahrens T; Kon S; Maeda M; Hotta H; Uede T; Simon JC. 2001. Osteopontin is involved in the initiation of cutaneous contact hypersensitivity by inducing Langerhans and dendritic cell migration to lymph nodes. J Exp Med 194(9):1219-29. [PubMed: 11696588] [MGI Ref ID J:119298]
Wesson JA; Johnson RJ; Mazzali M; Beshensky AM; Stietz S; Giachelli C; Liaw L; Alpers CE; Couser WG; Kleinman JG; Hughes J. 2003. Osteopontin is a critical inhibitor of calcium oxalate crystal formation and retention in renal tubules. J Am Soc Nephrol 14(1):139-47. [PubMed: 12506146] [MGI Ref ID J:103140]
Wilson MJ; Liaw L; Koopman P. 2005. Osteopontin and related SIBLING glycoprotein genes are expressed by Sertoli cells during mouse testis development. Dev Dyn 233(4):1488-95. [PubMed: 15937924] [MGI Ref ID J:99574]
Wolak T; Kim H; Ren Y; Kim J; Vaziri ND; Nicholas SB. 2009. Osteopontin modulates angiotensin II-induced inflammation, oxidative stress, and fibrosis of the kidney. Kidney Int 76(1):32-43. [PubMed: 19357716] [MGI Ref ID J:166277]
Xanthou G; Alissafi T; Semitekolou M; Simoes DC; Economidou E; Gaga M; Lambrecht BN; Lloyd CM; Panoutsakopoulou V. 2007. Osteopontin has a crucial role in allergic airway disease through regulation of dendritic cell subsets. Nat Med 13(5):570-8. [PubMed: 17435770] [MGI Ref ID J:164491]
Yang H; Guo H; Fan K; Zhang B; Zhao L; Hou S; Qian W; Zhang D; Wang H; Dai J; Guo Y. 2011. Clearance of Propionibacterium acnes by kupffer cells is regulated by osteopontin through modulating the expression of p47phox. Mol Immunol 48(15-16):2019-26. [PubMed: 21737140] [MGI Ref ID J:177212]
Yoo KH; Thornhill BA; Forbes MS; Coleman CM; Marcinko ES; Liaw L; Chevalier RL. 2006. Osteopontin regulates renal apoptosis and interstitial fibrosis in neonatal chronic unilateral ureteral obstruction. Kidney Int 70(10):1735-41. [PubMed: 17003824] [MGI Ref ID J:136483]
Health & husbandry
Health & Colony Maintenance Information
Animal Health Reports
Room Number AX12
Colony Maintenance
Breeding & Husbandry This strain originated on a mixed Black Swiss, 129S6 background and has been backcrossed to C57BL/6 for at least 10 generations (March 2003). The strain is maintained as a homozygote. Mating System Homozygote x Homozygote (Female x Male) 01-MAR-06 Diet Information LabDiet® 5K52/5K67
Purchasing information
Pricing, Supply Level & Notes, Controls
| Pricing for USA, Canada and Mexico shipping destinations |
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 |
Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $125.00 Female or Male Homozygous for Spp1tm1Blh
Pairs /Price (US dollars $) Pair Genotype $250.00 Homozygous for Spp1tm1Blh x Homozygous for Spp1tm1Blh Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
| Pricing for International shipping destinations |
|
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Live Mice
Price (US dollars $) Gender Genotypes Provided Individual Mouse $162.50 Female or Male Homozygous for Spp1tm1Blh
Pairs /Price (US dollars $) Pair Genotype $325.00 Homozygous for Spp1tm1Blh x Homozygous for Spp1tm1Blh Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
|
|
|
Standard Supply
Repository-Live. The Repository Strains represent an exclusive set of over 1500 unique mouse models maintained at The Jackson Laboratory to support a vast array of research areas. The breeding colonies for Repository Strains provide mice for both large and small orders and fluctuate in size depending on current demand for each strain. We treat orders for these strains as custom orders. Within 2 business days, we respond to each availability inquiry or order with various delivery options. Repository Strains typically are delivered at 4 to 8 weeks of age and will not exceed 12 weeks of age on the day of shipping.
General Supply Notes
- This strain is included in the Induced Mutant Resource Colony collection.
- Genomic DNA is available for this strain from the Mouse DNA Resource.
Control Information
| Control | ||
|---|---|---|
| 000664 C57BL/6J | ||
| Considerations for Choosing Controls | ||
| Control Pricing Information for Genetically Engineered Mutant Strains. | ||
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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.Ordering Information
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Contact information
General inquiriesContracts Administration
| phone: | 207-288-6470 |
| fax: | 207-288-6655 |
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
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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.
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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.