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Endocrinology, doi:10.1210/endo-125-3-1666
Endocrinology Vol. 125, No. 3 1666-1672
Copyright © 1989 by the Endocrine Society.
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Activin-A, Inhibin and Transforming Growth Factor-β Modulate Growth of Two Gonadal Cell Lines*

CONSUELO GONZALEZ-MANCHON and WYLIE VALE{dagger}

Clayton Foundation Laboratories for Peptide Biology, The Salk Institute La Jolla, California 92037

Address requests for reprints to: Dr. Wylie Vale, Peptide Biology Laboratory, The Salk Institute, P.O. Box 85800, San Diego, California 92138.

Abstract

The proliferative and differentiating effects of the gonadal hormones inhibin and activin-A were examined on cell lines derived from the ovary and testis. Activin-A was found to inhibit the growth of CHO-K1 (Chinese hamster ovary) cells in culture, with an IC50 of 3 ng/ml. The maximal response (50% inhibition) required 3 days of incubation in the presence of 40 ng/ml activin-A, and the inhibitory effect was accompanied by morphological changes. Inhibin (10 ng/ml) partially blocked the inhibition of growth by activin. Transforming growth factor-β (TGFβ), which is structurally related to activin and inhibin, was a very potent inhibitor of the proliferation of CHO-Kl cells, with an ICB0 of 0.2 ng/ml and a maximal effect (70% inhibition) at 2 ng/ml. The combination of high concentrations of both TGFβ and activin-A did not result in a greater inhibitory effect than that observed with TGFβ alone, suggesting an overlapping step in the mechanism of action for both factors.

In contrast to the results with CHO-Kl cells, differential effects of activin-A and TGFβ were observed in R2C (rat Leydig cell testicular tumor) cells. Activin-A had only a slight effect on proliferation over a 4-day incubation, but inhibited progesterone accumulation in a concentration-dependent fashion within 12 h. TGFβ, on the other hand, was a potent inhibitor of both growth and steroidogenesis in R2C cells.

These studies suggest that activin-A and inhibin may regulate proliferation as well as functions of gonadal cells.

Footnotes

* This work was supported by the Consejo Superior de Investigaciones Centificas (Madrid, Spain) and NIH Program Project Grant HD-13527. Research was conducted in part by the Clayton Foundation for Research, California Division.

{dagger} Clayton Foundation Investigator.

Received April 17, 1989.




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