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Proliferative Phase Sertoli Cells Display a Developmentally Regulated Response to Activin in Vitro

Monash Institute of Reproduction and Development (J.J.B., D.M.d.K., A.E.O’C., J.R.M.) and Department of Anatomy and Cell Biology (J.J.B., N.G.W.), Monash University; and Prince Henry’s Institute of Medical Research (P.G.F.), Clayton, Victoria 3168, Australia

Address all correspondence and requests for reprints to: John R Morrison, Monash Institute of Reproduction and Development, 27–31 Wright Street, Clayton, Victoria 3168, Australia. E-mail:john.morrison{at}med.monash.edu.au.

We have used cultures of highly purified, proliferating rat Sertoli cells collected from d 3, 6, and 9 rat pups to investigate the role of activin A on Sertoli cell division. These studies demonstrate that activin A acts directly on d 6 and 9, but not d 3, Sertoli cells to induce proliferation, both alone and synergistically with FSH. In addition to stimulating proliferation, activin A induces secretion of inhibins A and B as determined by specific ELISAs. We demonstrate that the synergy between activin A and FSH is not due to local actions of secreted inhibin or follistatin. We have used real-time fluorometric RT-PCR to demonstrate that activin regulates expression of activin receptor and follistatin mRNA by Sertoli cells. Saturation binding studies using ¹²⁵I-activin A indicate that synergy between activin and FSH may be due to increased numbers of activin receptors on the Sertoli cell. Finally, we show that activin A was secreted at high levels by cultured peritubular cells but was undetectable in high purity proliferating Sertoli cell cultures, suggesting that activin A functions as a paracrine factor during postnatal testis development.

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