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The Modulation of Gonadotrophs Hormone Action on the Ovary by Paracrine and Autocrine Factors
Author(s) -
Campbell BK
Publication year - 1999
Publication title -
reproduction in domestic animals
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.546
H-Index - 66
eISSN - 1439-0531
pISSN - 0936-6768
DOI - 10.1111/j.1439-0531.1999.tb01232.x
Subject(s) - endocrinology , medicine , paracrine signalling , biology , theca , autocrine signalling , ovary , growth factor , epidermal growth factor , ovarian follicle , follicle stimulating hormone , granulosa cell , luteinizing hormone , hormone , receptor
It has been hypothesized that the physiological basis of follicle selection is the differential expression of factors, that modulate the action of gonadotrophins on follicular cells, at key points during the process of follicle development. The aim of this research was to test this hypothesis by identifying factors that can enhance or attenuate the action of the gonadotrophins in stimulating follicle development using both in vivo and in vitro models. Experiments in vivo utilized sheep with an ovarian autotransplant to allow intra‐arterial infusion of putative local factors and exposure of the ovary to high local concentrations. Experiments in vitro utilized physiological serum‐free cell culture systems for both granulosa and theca cells that allow gonadotrophin‐induced differentiation in vitro. The putative local factors tested included insulin‐like growth factor‐I (IGF‐I LR3 analogue), transforming growth factor a (TGFα) or epidermal growth factor (EGF) and in‐hibin A. IGF‐I stimulated both cellular proliferation and hormone production by both granulosa and theca cells in vitro and similarly stimulated ovarian follicle development and ovarian androgen and oestradiol secretion in vivo. Both TGFα and EGF stimulated granulosa and thecal cell proliferation in vitro in a dose responsive manner and concomitantly inhibited hormone production whereas intra‐arterial infusion of TGFα in vivo resulted in induction of atresia in large antral follicles and an acute fall in ovarian hormone secretion. Inhibin A in vitro augmented gonadotrophin stimulated androgen and oestradiol production by thecal and granulosa cells respectively, but had no effect on cell number. Paradoxically, intra‐arterial infusion of inhibin A resulted in an acute depression in ovarian steroid secretion. This depression, however, was also associated with an acute depression in circulating FSH concentrations. In conclusion, these data provide strong support for the hypothesis that factors can modulate the action of gonadotrophins on follicular cells to augment (IGF‐I, inhibin A) or inhibit (TGFα/EGF) granulosa and thecal cell differentiation. The challenge for the future in this area of research is to understand how these factors interact to enable one follicle to be selected from an ovulatory cohort.