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Molecular Human Reproduction, Vol. 7, No. 5, 415-423, May 2001
© 2001 European Society of Human Reproduction and Embryology

Ovary and oogenesis

Distinct regulation of gene expression by prostaglandin F2{alpha} (PGF2{alpha}) is associated with PGF2{alpha} resistance or susceptibility in human granulosa-luteal cells

Shaw-Jenq Tsai1,3, Meng-Hsing Wu2, Pei-Chin Chuang1 and Hsiu-Mei Chen1

1 Departments of Physiology and 2 Obstetrics & Gynecology, National Cheng Kung University Medical College, Tainan 701, Taiwan, Republic of China

Abstract

The effects of human chorionic gonadotrophin (HCG) and prostaglandin F2{alpha} (PGF2{alpha}) 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 PGF2{alpha}) 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 PGF2{alpha} (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, PGF2{alpha} 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 PGF2{alpha}-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 PGF2{alpha}-induced luteolysis.

FP/granulosa-luteal cell/LH receptor/PGF2{alpha}/PGHS-2

Notes

3 To whom correspondence should be addressed. E-mail: Seantsai{at}mail.ncku.edu.tw


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