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Willem. S. Pretorius1 *, Willem. A. Coetzer1 , Danie M. Barry1 *
Department of Human and Animal Physiology, University of Stellenbosch, Stellenbosch, South Africa 1
Estrogen (E2) is luteolytic during the first 5 days of the estrous cycle in the ewe despite the fact that it is considered a mitogenic hormone. Very high levels of E2 have been implicated as the cause of premature luteal regression in the superovulated ewe. Up to now it was assumed that E2 induces luteal regression via the up-regulation of oxytocin receptors, resulting in the release of a luteolytic amount of prostaglandin F2 (PGF2). Premature luteal regression, however, presents some characteristics that are not found in PGF2 induced regression, including the occurrence of ovaries with both normal functioning and regressed corpora lutea. The question arises if E2 always exerts its luteolytic action via PGF2, or can it cause luteolysis by acting directly on luteal cells. We used in vitro culture of granulosa cells studying the direct effects of E2 on luteal cells in the absence of PGF2. Results have shown that E2 can cause a reduction in progesterone production in granulosa cells cultured from small follicles (< 5 mm in diameter) but not in granulosa cells from larger follicles (> 5 mm in diameter) (P< 0.001). This effect could be prevented by the administration of Long-R3-insulin like growth factor-I (long-R3-ILGF-I) to cultures (P< 0.001). It was found that granulosa cells from larger follicles lack estrogen receptors (ER) after 6 days of culture in vitro while granulosa cells from small follicles still have ER present. Long-R3-ILGF-I treated granulosa cells from small follicles lacked ER. Thus we concluded that Long-R3-ILGF-I prevented E2 induced reduction in progesterone synthesis, by down regulating ER.
This abstract is being presented on Sunday, August 1 at 8:00 AM to 10:15 AM at CUB 2nd Floor Ballroom.