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      Distinct regulation of gene expression by prostaglandin F(2alpha) (PGF(2alpha)) is associated with PGF(2alpha) resistance or susceptibility in human granulosa-luteal cells.

      Molecular Human Reproduction
      Cell Division, Cells, Cultured, Chorionic Gonadotropin, pharmacology, Cyclooxygenase 2, Dinoprost, Female, Gene Expression Regulation, drug effects, Granulosa Cells, metabolism, Humans, Isoenzymes, biosynthesis, genetics, Luteal Cells, Membrane Proteins, Progesterone, Prostaglandin-Endoperoxide Synthases, RNA, Messenger, Receptors, LH, Receptors, Prostaglandin

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          Abstract

          The effects of human chorionic gonadotrophin (HCG) and prostaglandin F(2alpha) (PGF(2alpha)) on regulation of human granulosa-luteal cell (GLC) function at different stages of differentiation (day 2 versus day 8 of culture) were studied. Expression of LH receptor mRNA and biosynthesis of progesterone were HCG dependent in human GLC at all stages (n = 6, P < 0.05). Steady-state concentrations of mRNA encoding for FP (a specific high-affinity plasma membrane receptor for PGF(2alpha)) were not dependent on, but were stimulated by, addition of HCG (10 IU/ml) or 8-bromo-cAMP (0.5 mmol/l) (n = 6, P < 0.05). Treatment with PGF(2alpha) (100 nmol/l) decreased FP mRNA concentration, but had no effect on LH receptor and cyclo oxygenase-2 (COX-2) expression on day 2 of cultured GLC (n = 8). As a result, the progesterone biosynthesis by GLC was not affected. On day 8, PGF(2alpha) induced FP and PGHS-2 expression and at the same time decreased LH receptor expression, resulting in inhibition of progesterone output by GLC. Our data demonstrated that early stage GLC (day 2 of culture) are resistant to PGF(2alpha)-induced inhibition of progesterone synthesis but underwent further differentiation and acquired luteolytic capacity after 8 days culture in vitro. We conclude that, via distinct gene regulation at different stages of differentiation, human GLC may become resistant or susceptible to PGF(2alpha)-induced luteolysis.

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