ArticleThe American journal of pathology2004
A locus on chromosome 7 determines dramatic up-regulation of osteopontin in dystrophic cardiac calcification in mice.
Article in The American journal of pathology, 2004. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.
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Who cites it
19 citing papers in PubMed.
- Elevated phosphate levels in CKD - a direct threat for the heart.Nephrology, dialysis, transplantation : official publication of the European Dialysis and Transplant Association - European Renal Association · 2025Review
- ABCC6, Pyrophosphate and Ectopic Calcification: Therapeutic Solutions.International journal of molecular sciences · 2021Review
- Article
- Dietary Pyrophosphate Modulates Calcification in a Mouse Model of Pseudoxanthoma Elasticum: Implication for Treatment of Patients.The Journal of investigative dermatology · 2019Article
- C.B-17 SCID mice develop epicardial calcinosis with unaltered cardiac function.Fundamental & clinical pharmacology · 2019Article
- Etidronate prevents dystrophic cardiac calcification by inhibiting macrophage aggregation.Scientific reports · 2018Article
- The ABCC6 Transporter: A New Player in Biomineralization.International journal of molecular sciences · 2017Review
- Pyrophosphate Supplementation Prevents Chronic and Acute Calcification in ABCC6-Deficient Mice.The American journal of pathology · 2017Article
- Cardiac Fibroblasts Adopt Osteogenic Fates and Can Be Targeted to Attenuate Pathological Heart Calcification.Cell stem cell · 2017Article
- Disseminated arterial calcification and enhanced myogenic response are associated with abcc6 deficiency in a mouse model of pseudoxanthoma elasticum.Arteriosclerosis, thrombosis, and vascular biology · 2014Article
- The level of hepatic ABCC6 expression determines the severity of calcification after cardiac injury.The American journal of pathology · 2014Article
- Spontaneous cardiac calcinosis in BALB/cByJ mice.Comparative medicine · 2013Article
- New insights into the pathogenesis of pseudoxanthoma elasticum and related soft tissue calcification disorders by identifying genetic interactions and modifiers.Frontiers in genetics · 2013Article
- Development of autoimmune hair loss disease alopecia areata is associated with cardiac dysfunction in C3H/HeJ mice.PloS one · 2013Article
- The molecular and physiological roles of ABCC6: more than meets the eye.Frontiers in genetics · 2012Article
- Respiratory infection with Francisella novicida induces rapid dystrophic cardiac calcinosis (DCC).FEMS immunology and medical microbiology · 2008Article
- Identification of Abcc6 as the major causal gene for dystrophic cardiac calcification in mice through integrative genomics.Proceedings of the National Academy of Sciences of the United States of America · 2007Article
- Clinical manifestations and pathogenesis of hydroxyapatite crystal deposition in juvenile dermatomyositis.Current rheumatology reports · 2006Review
- Calcification of myocardial necrosis is common in mice.Virchows Archiv : an international journal of pathology · 2006Article
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9 authors.
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Abstract
Calcification of necrotic tissue is frequently observed in chronic inflammation and atherosclerosis. A similar response of myocardium to injury, referred to as dystrophic cardiac calcinosis (DCC), occurs in certain inbred strains of mice. We now examined a putative inhibitor of calcification, osteopontin, in DCC after transdiaphragmal myocardial freeze-thaw injury. Strong osteopontin expression was found co-localizing with calcification in DCC-susceptible strain C3H/HeNCrlBr, which exhibited low osteopontin plasma concentrations otherwise. Osteopontin mRNA induction was 20-fold higher than in resistant strain C57BL/6NCrlBr, which exhibited fibrous lesions without calcification and little osteopontin expression. Sequence analysis identified several polymorphisms in calcium-binding and phosphorylation sites in osteopontin cDNA. Their potential relevance for DCC was tested in congenic mice, which shared the osteopontin locus with C57BL/6NCrlBr, but retained a chromosomal segment from C3H/HeNCrlBr on proximal chromosome 7. These mice exhibited strong osteopontin expression and DCC comparable to C3H/HeNCrlBr suggesting that a trans-activator of osteopontin transcription residing on chromosome 7 and not the osteopontin gene on chromosome 5 was responsible for the genetic differences in osteopontin expression. A known osteopontin activator encoded by a gene on chromosome 7 is the transforming growth factor-beta1, which was more induced (3.5x) in C3H/HeNCrlBr than in C57BL/6NCrlBr mice.
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