Wu W X, Ma X H, Yoshizato T, Shinozuka N, Nathanielsz P W
Laboratory for Pregnancy and Newborn Research, Department of Biomedical Sciences, College of Veterinary Medicine, Cornell University, Ithaca, New York 14853-6401, USA.
J Soc Gynecol Investig. 2001 Mar-Apr;8(2):69-76.
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.
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.
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.
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.
前列腺素F合酶（PGFS）催化前列腺素H2还原为前列腺素F2α。目前尚无关于任何物种孕期子宫组织中PGFS mRNA或蛋白质表达及调控与分娩关系的信息。我们使用克隆的绵羊PGFS核糖探针，对倍他米松诱导的早产和自然足月分娩时绵羊子宫肌层、子宫内膜、母体和胎儿胎盘组织中的PGFS mRNA表达进行了特征分析。同时评估前列腺素H合酶（PGHS）2 mRNA作为对照，其与妊娠相关的变化已为人熟知。
分析来自妊娠143 - 147天（dGA，TCNL，n = 6）的对照母羊、145 - 147 dGA自然足月分娩母羊（STL，n = 6）、未分娩的早期对照母羊（ECNL，n = 6）以及128 - 135 dGA倍他米松诱导分娩母羊（BL，n = 6）的胎儿胎盘、子宫肌层和子宫内膜的多聚A或总RNA中的PGHS2和PGFS mRNA。
子宫肌层、子宫内膜和胎儿胎盘在自然足月分娩时PGFS mRNA无变化。在倍他米松诱导的早产过程中，子宫内膜和母体胎盘的PGFS mRNA下降（P < 0.05），但胎儿胎盘和子宫肌层中保持不变。在倍他米松诱导的早产和自然足月分娩过程中，子宫内膜、胎盘和子宫肌层中的PGHS2 mRNA增加。
PGHS2 mRNA增加而非PGFS mRNA增加与倍他米松诱导的早产以及子宫内膜、胎盘和子宫肌层的自然足月分娩的开始密切相关。PGFS mRNA的转录可能不是分娩时导致前列腺素F2α增加途径中的限速步骤。
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