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a Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3
b Department of Obstetrics and Gynecology, Gumma University, Maebashi, Japan
Activin A has been shown to exert several regulatory functions on human placenta. In the present study, we tested the hypothesis that activin A is an autocrine regulator of trophoblast using a choriocarcinoma cell line, JEG-3, as a model. Messenger RNAs for activin ßA subunit, activin binding protein (follistatin), and various activin receptors, including ActR-IA, ActR-IB, ActR-IIA, and ActR-IIB, were detected in JEG-3 cells by reverse transcription-polymerase chain reaction. The expression of activin A in JEG-3 cells was further confirmed by Western blot analysis using an antibody against activin ßA subunit. Using Northern blot analysis, Smad-2 and Smad-4 mRNAs were also observed in JEG-3 cells. These data suggest that JEG-3 cells produce activin A and express activin binding proteins and receptors, as well as potential downstream signals. In cultured JEG-3 cells, basal progesterone production was stimulated by activin A but inhibited by follistatin-288. Similarly, in the presence of androstenedione, estradiol production was enhanced by activin A but decreased by follistatin-288. On the other hand, neither activin A nor follistatin affected JEG-3 cell growth. Taken together, these findings strongly suggest that activin A is an autocrine factor that is involved in the regulation of progesterone and estradiol production in JEG-3 cells.
1 This study was supported by a grant from Medical Research Council of Canada to C.P. C.P. is a recipient of Women's Faculty Awards from the Natural Sciences and Engineering Research Council of Canada. Some preliminary results have been presented as a poster at the 80th Annual Meeting of the Endocrine Society; June 23–27, 1998; New Orleans, LA.
2 Correspondence: Chun Peng, Department of Biology, York University, 4700 Keele St., Toronto, ON, Canada M3J 1P3. FAX: 416 736 5698; cpeng{at}yorku.ca
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