Mediators of maternal recognition of pregnancy in mammals.
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Maternal recognition of pregnancy results from signaling between the conceptus (embryo and its associated membranes) and the maternal system (1). These signals ensure maintenance of structural and functional integrity of the corpus luteum (CL), which would otherwise regress at the end of the estrous of menstrual cycle. The CL produces progesterone, the hormone of pregnancy, which is required to stimulate and maintain endometrial functions that are permissive to early embryonic development, implantation, placentation, and successful fetal and placental development. The terms luteotrophic, luteal protective, antiluteolytic, and luteolytic will be defined before mechanisms for maternal recognition of pregnancy are discussed. A luteotrophic signal, e.g., chorionic gonadotrophin (CG), is produced by primate conceptuses, and appears to act directly on the CL, via receptors for luteinizing hormone, to ensure maintenance of its structural and functional integrity. It is important to keep in mind that the ovarian cycle of primates is uterine independent, i.e., luteolytic events responsible for regression of the CL and cessation of progesterone secretion at the end of a menstrual cycle result from intraovarian effects of prostaglandins, oxytocin, or other, as yet undefined, luteolytic agents. A luteolytic agent causes structural and functional demise of the CL or luteolysis. Prostaglandin (PG) F2 is the luteolytic signal common to most, if not all, mammals. There may also be luteal protective signals, e.g., PGE2 (PGE), that antagonize potential luteolytic effects of PGF. The ovarian cycle of subprimate mammals is uterine dependent and hysterectomy extends CL maintenance for a period characteristic of the species'gestational period. The uterine endometrium, primarily surface epithelium and perhaps superficial glandular epithelium, produces PGF, which is responsible for luteolysis. Signals from conceptuses of subprimate mammals are termed antiluteolytic because they either inhibit endometrial release of luteolytic amounts of PGF or alter the pattern of endometrial secretion of PGF to abrogate its luteolytic effects. 1992, SAGE Publications. All rights reserved.
