Transforming growth factor β1 regulates follistatin mrna expression during in vitro bovine granulosa cell differentiation

✍ Scribed by Monica Fazzini; Griselda Vallejo; Alejandro Colman-Lerner; Romina Trigo; Stella Campo; J. Lino S. Barañao; Patricia E. Saragüeta

• Publisher: John Wiley and Sons
• Year: 2006
• Tongue: English
• Weight: 278 KB
• Volume: 207
• Category: Article
• ISSN: 0021-9541
• DOI: 10.1002/jcp.20533

✦ Synopsis

Abstract

In order to test the hypothesis that transforming growth factor β (TGF‐β) acts by FS regulation on bovine granulosa cells in in vitro differentiation, we analyzed the effect of TGF‐β1 on follistatin mRNA expression in three differentiation states of bovine granulosa cells. We showed a positive regulation of FS mRNA after TGF‐β1 (1 ng/ml) treatment of freshly isolated granulosa cells from small‐medium antral follicles (2–8 mm). This effect was abolished by the addition of exogenous follistatin (100 ng/ml), suggesting that this effect could be mediated by activin. Although these cells showed a similar effect on FS mRNA expression after treatment with activin‐A, a soluble form of activin receptor type IIA was unable to inactivate the TGF‐β effect. When we tested the TGF‐β effect on FS mRNA in different granulosa cell states, TGF‐β1 regulation was associated with progesterone production only in freshly isolated cells. The amount of total activin‐A produced by first passage cells (dedifferentiated cells), was ten times smaller than the one measured in a conditioned medium from freshly isolated cells (mature cells). The TGF‐β1‐dependent FS mRNA expression persisted in first passage cells without changes with FS addition. On the other hand, the BGC‐1 granulosa cell line (immature cells) produced large amounts of activin‐A regulated by TGF‐β1 and an invariable steady state of FS mRNAs. In summary, our results showed that FS mRNA expression is regulated by TGF‐β1 independently of activin effects in differentiated granulosa cells. J. Cell. Physiol. 207: 40–48, 2006. © 2005 Wiley‐Liss, Inc.