The roles of activins, inhibins and estrogen in early committed follicles

The hypothesis that activin and inhibin are autocrine/paracrine mediators o f ovarian folliculogenesis has a solid basis. In mouse and rat models, gran ulosa cells (GC) of committed follicles express mRNA and protein for the ac tivin/inhibin subunits and mRNA for the activin receptors (type I and II). Dimeric inhibin-A and -B are produced by postnatal ovarian cell dispersates and (GC) in culture. Similar levels of inhibin-A and -B are produced by po stnatal ovarian cells, but thereafter as the ovary develops, inhibin-A beco mes the predominant form. Activin was more effective than transforming grow th factor-beta (TGF-beta) in enhancing follicle stimulating hormone (FSH)-s timulated inhibin production by ovarian cells. Evidence for a local regulat ory role of estrogen in the ovary is also accumulating. Murine models of es trogen receptor (ER alpha or ER beta) disruption produce mice with abnormal ovarian phenotypes. Female mice, which lack the capacity to produce estrog en (ArKO mice), have arrested folliculogenesis, no corpora lutea, elevated levels of luteinising hormone (LH), FSH and testosterone and are infertile. These data are consistent with autocrine/paracrine actions of activin in t he early growth of committed follicles and estrogen in follicular maturatio n. (C) 2000 Elsevier Science Ireland Ltd. All rights reserved.