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Regular Article |
a Instituto de Biología y Medicina Experimental—CONICET and Facultad de Ciencias Exactas y Naturales, Universidad de Buenos Aires,1428 Buenos Aires, Argentina
We evaluated the effects of transforming growth factor ß1 (TGFß1), alone or in combination with FSH and estradiol, on DNA synthesis in primary cultures of immature rat granulosa cells. 3H-Thymidine incorporation was significantly stimulated by TGFß1 (5.6-fold). This effect was enhanced by FSH (20 ng/ml, 27.7-fold) or estradiol (100 ng/ml, 13.4-fold) or by a combination of both hormones (59.2-fold). Measurement of TGFß bioactivity showed the presence of significant amounts of TGFß in conditioned medium from granulosa cell cultures, and most of the activity was present in the latent form. FSH alone or in combination with estradiol produced a marked suppression of the production of latent and active TGFß. Activated conditioned medium from control cultures of granulosa cell elicited a 1.4-fold increase in thymidine incorporation. This effect was markedly amplified by FSH (3-fold) and estradiol (4.3-fold) and by a combination of both (8.7-fold). The peptide containing the cell-binding domain of fibronectin (RGDSPC) partially inhibited thymidine incorporation stimulated by TGFß1. Fibronectin did not synergize with FSH, and the interaction between TGFß1 and FSH was even observed in the presence of this protein. The conclusions reached were as follows: 1) TGFß1 is an autocrine stimulator of rat granulosa cell DNA synthesis, 2) FSH and estradiol produce a suppression of latent and active TGFß production but markedly amplify TGFß action, presumably at a postreceptor level, and 3) the stimulatory effects of TGFß1 may be only partly mediated by the increased fibronectin secretion.
1 This work was supported by grants from CONICET, the Buenos Aires University (TX218 to J.L.B.), and a Carrillo Oñativia Fellowship to J.L.B.
2 Correspondence: Patricia Saragüeta, Obligado 2490, 1428 Buenos Aires, Argentina. FAX: 54 11 4786 2564; sarag{at}dna.uba.ar
3 These authors contributed equally to this work
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