The classic receptor for 1α,25-dihydroxy vitamin D3 is required for non-genomic actions of 1α,25-dihydroxy vitamin D3 in osteosarcoma cells

✍ Scribed by Soraya Bravo; Roberto Paredes; Pamela Izaurieta; Jane B. Lian; Janet L. Stein; Gary S. Stein; Maria Victoria Hinrichs; Juan Olate; Luis G. Aguayo; Martin Montecino

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 110 KB
• Volume: 99
• Category: Article
• ISSN: 0730-2312
• DOI: 10.1002/jcb.21031

✦ Synopsis

1a,25-dihydroxy vitamin D3 has a major role in the regulation of the bone metabolism as it promotes the expression of key bone-related proteins in osteoblastic cells. In recent years it has become increasingly evident that in addition to its well-established genomic actions, 1a,25-dihydroxy vitamin D3 induces non-genomic responses by acting through a specific plasma membrane-associated receptor. Results from several groups suggest that the classical nuclear 1a,25-dihydroxy vitamin D3 receptor (VDR) is also responsible for these non-genomic actions of 1a,25-dihydroxy vitamin D3. Here, we have used siRNA to suppress the expression of VDR in osteoblastic cells and assessed the role of VDR in the non-genomic response to 1a,25-dihydroxy vitamin D3. We report that expression of the classic VDR in osteoblasts is required to generate a rapid 1a,25-dihydroxy vitamin D3-mediated increase in the intracellular Ca 2þ concentration, a hallmark of the non-genomic actions of 1a,25-dihydroxy vitamin D3 in these cells.