title: Activin A in JEG-3 cells: potential role as an autocrine regulator of steroidogenesis in humans.
abstract: 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 beta(A) 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 beta(A) 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.
authors.affiliation: Department of Biology, York University, Toronto, Ontario, Canada M3J 1P3. Department of Obstetrics and Gynecology, Gumma University, Maebashi, Japan.
authors.forename: X
authors.initials: X
authors.lastname: Ni
authors.forename: S
authors.initials: S
authors.lastname: Luo
authors.forename: T
authors.initials: T
authors.lastname: Minegishi
authors.forename: C
authors.initials: C
authors.lastname: Peng
mesh_terms: D029404:Activin Receptors; D028341:Activins; D019898:Autocrine Communication; D002455:Cell Division / Q000187:drug effects; D002822:Choriocarcinoma; D004268:DNA-Binding Proteins / Q000235:genetics / Q000378:metabolism; D004958:Estradiol / Q000096:biosynthesis; D038681:Follistatin; D006023:Glycoproteins / Q000378:metabolism / Q000494:pharmacology; D006801:Humans; D007265:Inhibins / Q000378:metabolism* / Q000494:pharmacology; D011374:Progesterone / Q000096:biosynthesis; D017978:Receptors, Growth Factor / Q000235:genetics / Q000378:metabolism; D051899:Smad2 Protein; D051901:Smad4 Protein; D013256:Steroids / Q000378:metabolism*; D013997:Time Factors; D015534:Trans-Activators / Q000235:genetics / Q000378:metabolism; D014327:Trophoblasts / Q000378:metabolism*; D014407:Tumor Cells, Cultured
chemical_list: D004268:DNA-Binding Proteins; D038681:Follistatin; D006023:Glycoproteins; D017978:Receptors, Growth Factor; C497782:SMAD2 protein, human; C497796:SMAD4 protein, human; D051899:Smad2 Protein; D051901:Smad4 Protein; D013256:Steroids; D015534:Trans-Activators; D028341:Activins; D011374:Progesterone; D004958:Estradiol; D007265:Inhibins; D029404:Activin Receptors