Increase in prostaglandin H synthase 2, but not prostaglandin F2alpha synthase mRNA in intrauterine tissues during betamethasone-induced premature labor and spontaneous term labor in sheep

Abstract

Objective: Prostaglandin F synthase (PGFS) catalyzes reduction of prostaglandin H(2) to PGF2alpha. No information exists on PGFS expression and regulation during pregnancy, either mRNA or protein, in relation to labor in uterine tissues in any species. We characterized PGFS mRNA expression in ovine myometrium, endometrium, maternal and fetal placenta in betamethasone-induced premature labor and spontaneous term labor using our cloned ovine PGFS riboprobe. Prostaglandin H synthase (PGHS) 2 mRNA was evaluated simultaneously as a control whose pregnancy related changes are well known.

Methods: Poly-A or total RNA from fetal placenta, myometrium, and endometrium in control ewes at 143-147 days of gestational age (dGA, TCNL, n = 6), and ewes in spontaneous term labor at 145-147 dGA (STL, n = 6) and endometrium and maternal and fetal placenta in early control ewes not in labor (ECNL, n = 6) and betamethasone induced labor at 128-135 dGA (BL, n = 6) were analyzed for PGHS2 and PGFS mRNA.

Results: PGFS mRNA did not change at spontaneous term labor in myometrium, endometrium, and fetal placenta. PGFS mRNA decreased during betamethasone-induced premature labor in endometrium and maternal placenta (P < .05), but remained unchanged in fetal placenta and myometrium. PGHS2 mRNA increased in endometrium, placenta, and myometrium during betamethasone-induced premature labor and spontaneous term labor.

Conclusion: Increased PGHS2, but not PGFS mRNA was tightly associated with the onset of betamethasone-induced premature labor as well as spontaneous term labor in the endometrium, placenta, and myometrium. Transcription of PGFS mRNA may not be the rate-limiting step in the pathway contributing to increased PGF(2alpha) at labor.