Ontology type: schema:ScholarlyArticle Open Access: True
2006-11
AUTHORSJian Q Feng, Leanne M Ward, Shiguang Liu, Yongbo Lu, Yixia Xie, Baozhi Yuan, Xijie Yu, Frank Rauch, Siobhan I Davis, Shubin Zhang, Hector Rios, Marc K Drezner, L Darryl Quarles, Lynda F Bonewald, Kenneth E White
ABSTRACTThe osteocyte, a terminally differentiated cell comprising 90%-95% of all bone cells, may have multiple functions, including acting as a mechanosensor in bone (re)modeling. Dentin matrix protein 1 (encoded by DMP1) is highly expressed in osteocytes and, when deleted in mice, results in a hypomineralized bone phenotype. We investigated the potential for this gene not only to direct skeletal mineralization but also to regulate phosphate (P(i)) homeostasis. Both Dmp1-null mice and individuals with a newly identified disorder, autosomal recessive hypophosphatemic rickets, manifest rickets and osteomalacia with isolated renal phosphate-wasting associated with elevated fibroblast growth factor 23 (FGF23) levels and normocalciuria. Mutational analyses showed that autosomal recessive hypophosphatemic rickets family carried a mutation affecting the DMP1 start codon, and a second family carried a 7-bp deletion disrupting the highly conserved DMP1 C terminus. Mechanistic studies using Dmp1-null mice demonstrated that absence of DMP1 results in defective osteocyte maturation and increased FGF23 expression, leading to pathological changes in bone mineralization. Our findings suggest a bone-renal axis that is central to guiding proper mineral metabolism. More... »
PAGES1310-1315
http://scigraph.springernature.com/pub.10.1038/ng1905
DOIhttp://dx.doi.org/10.1038/ng1905
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