Abstract
Transforming growth factor-.beta. (TGF.beta.) has a differential effect on the growth and function of bovine adrenocortical cells in vitro. TGF.beta. inhibits basal as well as ACTH- or angiotensin II-stimulated steroid formation, with no evidence of change in cell growth. The major inhibitory effect of TGF.beta. occurs at a step before cholesterol formation, since treatment of adrenocortical cells with TGF.beta. decreased not only .DELTA.4-steroid levels but also .DELTA.5-steroid levels. The addition of cholesterol reverses the suppression of steroidogenesis induced by TGGF.beta.. To determine the mechanism of this inhibition the effect of TGF.beta. on low density lipoprotein (LDL) metabolism was investigated. Cells treated with TGF.beta. showed a significant suppression of [12I]iodohuman LDL ([125I]LDL) binding to the cell surface, followed by decreases in internalization and proteolytic degradation of [125I]LDL. Maximal inhibition of LDL metabolism was observed at a concentration of 1 ng/ml (4 .times. 10-11 M) TGF.beta.. The stimulation of LDL metabolism by ACTH was also inhibited by TGF.beta., and the inhibition observed correlated well with the inhibition of steroidogenesis. The inhibitory effect of TGF.beta. on [125I]LDL binding results from the decrease in the maximal LDL-binding capacity. The stimulation of LDL uptake induce by Bu2cAMP, cholera toxin, forskolin, and Ang II was also decreased by treatment with 1 ng/l TGF.beta.. The specificity of this effect is quite high, since the inhibitory effects of TGF.beta.v on LDL metabolism were not observed with either inhibin A or activin, two molecules that have considerable structural homology to TGF.beta.. We conclude that TGF.beta. specifically suppresses LDL metabolism in bovine adrenortical cell cultures and that this step may mediate, at least in part, its role as a potent inhibitor of steroidogenesis.

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