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Mol Cell Endocrinol. 2011 Dec 5;347(1-2):48-54. doi: 10.1016/j.mce.2011.05.018. Epub 2011 Jun 1.

Vitamin D metabolism, cartilage and bone fracture repair.

Author information

1
Genetics Unit, Shriners Hospital for Children, Montreal, Quebec, Canada H3G 1A6. rst-arnaud@shriners.mcgill.ca

Abstract

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.

PMID:
21664253
DOI:
10.1016/j.mce.2011.05.018
[Indexed for MEDLINE]

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