Agents affecting adenylate cyclase activity modulate the stimulatory action of 1,25-dihydroxyvitamin D3 on the production of osteocalcin by human bone cells.

Biochemical and Biophysical Research Communications
D B EvansP R Dobson

Abstract

The stimulation of osteocalcin synthesis by human osteoblast-like cells in response to 1,25-dihydroxyvitamin D3 (1,25(OH)2D3) is antagonised by several bone regulatory agents. We have shown that agents which activate adenylate cyclase inhibit this action of 1,25(OH)2D3 on human osteoblast-like cells. Activation of adenylate cyclase, either via the stimulatory GTP-binding protein using cholera toxin, or directly at the catalytic via the stimulatory GTP-binding protein using cholera toxin, or directly at the catalytic subunit using forskolin, results in a suppression of osteocalcin synthesis. Whilst the activation of adenylate cyclase induces this inhibitory response, neither exogenous dibutyryl cyclic AMP nor the phosphodiesterase inhibitor, IBMX, exerted any apparent effect on the production of osteocalcin. The tumour promoting phorbol ester, 4 beta-phorbol 12,13-dibutyrate, also inhibited 1,25(OH)2D3-stimulated osteocalcin production. This was not apparent in response to the non-tumour promoting phorbol ester 4 beta-phorbol suggesting the involvement of protein kinase C.

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Citations

Sep 1, 1992·Osteoporosis International : a Journal Established As Result of Cooperation Between the European Foundation for Osteoporosis and the National Osteoporosis Foundation of the USA·J P PraetP Bourdoux
Mar 29, 1991·Biochemical and Biophysical Research Communications·D B EvansJ A Kanis
Jan 1, 1991·Critical Reviews in Clinical Laboratory Sciences·M J Power, P F Fottrell
Dec 11, 2003·American Journal of Physiology. Endocrinology and Metabolism·Frank BarlettaSylvia Christakos

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