Studies on phosphatidylinositol metabolism and dexamethasone inhibition of proliferation of human palatal mesenchyme cells.

Abstract

The relationship between dexamethasone (DEX)-induced phosphatidylinositol (PI) turnover and inhibition of cell proliferation was investigated in human embryonic palatal mesenchyme (HEPM) cells in culture. Evidence based on studies with the partial glucocorticoid agonist cortexolone suggests both the PI response and the inhibition of proliferation are mediated by the glucocorticoid receptor. The role of PI turnover in the mechanism of DEX-inhibited HEPM cell proliferation was investigated using two agents that stimulated PI turnover (serum and platelet-derived growth factor) and one that did not stimulate PI turnover (epidermal growth factor). DEX partially inhibited both serum-induced and platelet-derived growth factor-induced proliferation of HEPM but not epidermal growth factor-induced proliferation. These results suggest that DEX-induced alteration of PI metabolism may be involved in the mechanism by which DEX inhibits proliferation of cultured HEPM cells and results in cleft palate formation in rodents.