Effects of corticosterone on Ca2+ uptake and myofibrillar disassembly in primary muscle cell culture.

Abstract

This study was done to examine the effects of corticosterone, a glucocorticoid, on Ca2+ uptake, proteolysis, and Ca2+ channels in primary cultures of chick muscle cells, to clarify the mechanism of glucocorticoid action on muscle proteolysis. Chick muscle cells were incubated for 24 h in a medium containing corticosterone (30 ng/ml) when the cells were confluent (6 days). To examine the contribution of Ca2+ channels, nifedipine, a Ca2+ channels antagonist, was used. Ca2+ uptake measured with 45CaCl2 was increased three-fold by corticosterone, with a peak at 12 h after the treatment started. The growth of the cells estimated from the protein content and creatine kinase activity was not affected by corticosterone. Proteolysis, evaluated with [3H]tyrosine as a label of the protein and Ntau-methylhistidine release, was unchanged by corticosterone. However, the amount of easily releasable myofilament as a measure of myofibrillar disassembly in the muscle cells was increased by corticosterone, and prevented by nifedipine. These results show that corticosterone increases Ca2+ uptake and starts myofibrillar protein breakdown.