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Genomic and non-genomic effects of progesterone on prostaglandin (PG) F2α and PGE2 production in the bovine endometrium
Author(s) -
Mariko Kuse,
Ryosuke Sakumoto,
Kiyoshi Okuda
Publication year - 2015
Publication title -
reproduction fertility and development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.609
H-Index - 76
eISSN - 1448-5990
pISSN - 1031-3613
DOI - 10.1071/rd14490
Subject(s) - stromal cell , endometrium , medicine , luteal phase , follicular phase , endocrinology , prostaglandin , biology , corpus luteum , estrous cycle , bovine serum albumin , chemistry , microbiology and biotechnology , biochemistry , ovary
Progesterone (P4) acts through different actuating pathways called genomic and non-genomic pathways. Here we investigated whether P4 regulates prostaglandin (PG) F2? (PGF) and PGE2 production in bovine endometrium through different pathways. Cultured endometrial cells were exposed to P4 for a short time (5-20min) or bovine serum albumin (BSA)-conjugated P4 (P4-BSA) for 24h. Progesterone treatment for 24h stimulated PGE2 production in epithelial cells, but suppressed both PGF and PGE2 production and the expression of PG-metabolising enzymes including phospholipase A2 (PLA2) and cyclooxygenase-2 (COX2) in stromal cells. Short-term (5-20min) P4 treatment did not affect PLA2 or COX2 transcript levels in either cell type. P4-BSA increased PGF and PGE2 production only in epithelial cells. Nuclear P4 receptor mRNA expression in endometrium was higher at the follicular phase than at the early- to mid-luteal stages, whereas membrane P4 receptor mRNA expression did not change throughout the oestrous cycle. The overall results suggest that P4 controls PG production by inhibiting enzymes via a genomic pathway and by stimulating signal transduction via a non-genomic pathway. Consequently, P4 may protect the corpus luteum by attenuating PGF production in stromal cells and by increasing PGE2 secretion from epithelial cells.

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