17β-estradiol regulates prostaglandin E2 and F2α, synthesis and function in endometrial explants of cattle

Prostaglandins (PG) have primary functions in the reproductive tract, however, the mechanism of regulation of PG secretion in the endometrium is unclear. Estrogen as a predominant regulator of uterine functions during the mammalian estrous cycle and effects of estrogen on synthesis of PG and function in uterine tissues of cattle are not fully understood. In this study, there was evaluation of the concentration- and time-effects of 17 beta-estradiol on PG synthesis in endometrial explants of cattle, focusing on the secretion of prostaglandin E-2 (PGE(2)) and prostaglandin F-2 alpha, (PGF(2 alpha)) as well as relative abundance of mRNA transcript and protein for both the enzymes responsible for PGE(2) and PGF(2 alpha), synthesis, including prostaglandin-endoperoxide synthase 1 and 2 (PTGS1, PTGS2), PGE(2) synthase (PGES), PGF(2 alpha), synthase (PGFS), and carbonyl reductase (CBR1), and the receptors responsible for downstream PGE(2) (PTGER2, PTGER4) and PGF(2 alpha), (PTGFR) signaling. Results indicated that 17 beta-estradiol increased PGE(2) and PGF(2 alpha), production at concentrations ranging from 10(-11) to 10(-8) M. Furthermore, abundances of PTGS1, PTGS2, PGES, PGFS, PTGER2, PTGER4, and PTGFR mRNA transcripts and protein were greater immediately after 17 beta-estradiol treatment at almost all the concentrations, while these CBR1 abundances were less as a result of treatments with 17 beta-estradiol. These data support the hypothesis that estradiol modulates the synthesis and function of PG in the endometrium of cattle.