Sugimoto Y, Yamasaki A, Segi E, Tsuboi K, Aze Y, Nishimura T, Oida H, Yoshida N, Tanaka T, Katsuyama M, Hasumoto K, Murata T, Hirata M, Ushikubi F, Negishi M, Ichikawa A, Narumiya S
Department of Physiological Chemistry, Faculty of Pharmaceutical Sciences, Kyoto University, Kyoto 606, Japan.
Science. 1997 Aug 1;277(5326):681-3. doi: 10.1126/science.277.5326.681.
Mice lacking the gene encoding the receptor for prostaglandin F2alpha (FP) developed normally but were unable to deliver normal fetuses at term. Although these FP-deficient mice showed no abnormality in the estrous cycle, ovulation, fertilization, or implantation, they did not respond to exogenous oxytocin because of the lack of induction of oxytocin receptor (a proposed triggering event in parturition), and they did not show the normal decline of serum progesterone concentrations that precedes parturition. Ovariectomy at day 19 of pregnancy restored induction of the oxytocin receptor and permitted successful delivery in the FP-deficient mice. These results indicate that parturition is initiated when prostaglandin F2alpha interacts with FP in ovarian luteal cells of the pregnant mice to induce luteolysis.
缺乏前列腺素F2α（FP）受体编码基因的小鼠发育正常，但足月时无法产出正常胎儿。尽管这些缺乏FP的小鼠在发情周期、排卵、受精或着床方面未表现出异常，但由于缺乏催产素受体的诱导（这是分娩中一个假定的触发事件），它们对外源催产素无反应，且未表现出分娩前血清孕酮浓度的正常下降。在妊娠第19天进行卵巢切除术可恢复催产素受体的诱导，并使缺乏FP的小鼠成功分娩。这些结果表明，当前列腺素F2α与妊娠小鼠卵巢黄体细胞中的FP相互作用以诱导黄体溶解时，分娩开始。
