| First Author | St-Arnaud R | Year | 2011 |
| Journal | Mol Cell Endocrinol | Volume | 347 |
| Issue | 1-2 | Pages | 48-54 |
| PubMed ID | 21664253 | Mgi Jnum | J:184113 |
| Mgi Id | MGI:5320267 | Doi | 10.1016/j.mce.2011.05.018 |
| Citation | St-Arnaud R, et al. (2011) Vitamin D metabolism, cartilage and bone fracture repair. Mol Cell Endocrinol 347(1-2):48-54 |
| abstractText | The 1,25-(OH)(2)D metabolite mediates the endocrine actions of vitamin D by regulating in the small intestine the expression of target genes that play a critical role in intestinal calcium absorption. The major role of the vitamin D hormone on bone is indirect and mediated through its endocrine function on mineral homeostasis. However, genetic manipulation of the expression of Cyp27b1 or the VDR in chondrocytes strongly support a direct role for locally synthesized 1,25(OH)(2)D, acting through the VDR, in vascular invasion and osteoclastogenesis during endochondral bone development. Cells from the growth plate respond to the 24,25-(OH)(2)D and 1,25-(OH)(2)D metabolites in a cell maturation-dependent manner and the effects of 1,25-(OH)(2)D are thought to be mediated through binding to the membrane-associated receptor PDIA3 (protein disulfide isomerase associated 3). The physiological relevance of membrane-mediated 1,25-(OH)(2)D signaling is emerging and is discussed. Finally, preliminary results suggest that mice deficient for Cyp24a1 exhibit a delay in bone fracture healing and support a role for 24,25-(OH)(2)D in mammalian fracture repair. |
