Please use this identifier to cite or link to this item:
|Scopus||Web of Science®||Altmetric|
|Title:||Modulation of osteoclastic migration by metabolism of 25(OH)-vitamin D₃|
|Other Titles:||Modulation of osteoclastic migration by metabolism of 25(OH)-vitamin D3|
|Citation:||Journal of Steroid Biochemistry and Molecular Biology, 2013; 136(1):59-61|
|Publisher:||Pergamon-Elsevier Science Ltd|
|M. Kogawa, D.M. Findlay, P.H. Anderson, G.J. Atkins|
|Abstract:||We have reported the metabolism of 25(OH) vitamin D3 (25D) into active 1α,25(OH)2 vitamin D3 (1,25D) by osteoclasts derived from human peripheral blood mononuclear cells (PBMC), RAW 264.7cells or giant cell tumor of bone (GCT), which appears to optimize osteoclast differentiation but inhibit their activity. In this study, to elucidate the mechanism by which 25D reduces osteoclast resorption, we further examined the effect of 25D on osteoclast function by using GCT-derived osteoclasts. 25D treated cells on dentine slices resulted in decreased resorption volume and depth in 3D image analysis. Tartrate-resistant acid phosphatase (TRAP) has been reported to enhance the dephosphorylation of substrate binding proteins, resulting in reduced osteoclast attachment. Therefore, we next investigated the effect of 25D on cell migration. Treatment of GCT cells with 25D augmented cell migration, as determined by live cell imaging. These observations suggest that 25D metabolism by osteoclasts reduces their resorptive capacity, in part by modifying their surface adhesion and migration properties. This article is part of a Special Issue entitled "Vitamin D Workshop".|
|Keywords:||25-Hydroxyvitamin D₃; Osteoclast; Migration; Metabolism; Autocrine; Paracrine|
|Rights:||Crown Copyright © 2012|
|Appears in Collections:||Orthopaedics and Trauma publications|
Files in This Item:
There are no files associated with this item.
Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.