Meidan R, Milvae R A, Weiss S, Levy N, Friedman A
Department of Animal Sciences, Faculty of Agriculture, Food and Environmental Quality Sciences, Hebrew University of Jerusalem, Rehovot, Israel.
J Reprod Fertil Suppl. 1999;54:217-28.
The corpus luteum is a transient gland, which is only functional for 17-18 days in the cyclic cow or for up to 200 days in the pregnant cow. Regression of the corpus luteum is essential for normal cyclicity as it allows the development of a new ovulatory follicle, whereas prevention of luteolysis is necessary for the maintenance of pregnancy. Evidence acquired over the past three decades indicated that PGF2 alpha is the luteolytic hormone in ruminants. Nevertheless, the detailed mechanisms of PGF2 alpha action are just beginning to be clarified. A pivotal role for an endothelial cell product endothelin 1 (ET-1) has been documented in PGF2 alpha-induced luteal regression. ET-1 inhibited progesterone production by luteal cells in a dose-dependent manner via selective ET-1 binding sites (ETA). The inhibitory action of PGF2 alpha on progesterone secretion (in vivo and in vitro) was blocked by a selective ETA receptor antagonist. This implied that ET-1 (through ETA receptors present on steroidogenic cells) may have mediated the inhibitory effect of PGF2 alpha. The involvement of ET-1 in luteal regression was also suggested by the observation that the highest concentrations of ET-1 coincide with uterine PGF2 alpha surges. Furthermore, PGF2 alpha administration upregulated ET-1 expression within the corpus luteum. Later stages of luteal regression, which involve programmed cell death (PCD), are presumably mediated by immune cells. ET-1 may also be involved in this process by promoting leukocyte migration and stimulating macrophages to release tumour necrosis factor alpha (TNF alpha). The TNF alpha receptor type 1 (p55) is present on luteal cells (endothelial and steroidogenic cells) and could initiate PCD and the structural demise of the corpus luteum.
黄体是一个临时性腺体，在周期性发情的母牛中仅发挥功能17 - 18天，而在怀孕母牛中可长达200天。黄体退化对于正常的发情周期至关重要，因为它能使新的排卵卵泡发育，而防止黄体溶解对于维持妊娠是必要的。过去三十年获得的证据表明，前列腺素F2α是反刍动物的黄体溶解激素。然而，前列腺素F2α作用的详细机制才刚刚开始被阐明。内皮细胞产物内皮素1（ET - 1）在前列腺素F2α诱导的黄体退化中已被证明起关键作用。ET - 1通过选择性ET - 1结合位点（ETA）以剂量依赖的方式抑制黄体细胞产生孕酮。选择性ETA受体拮抗剂可阻断前列腺素F2α对孕酮分泌的抑制作用（体内和体外）。这意味着ET - 1（通过存在于类固醇生成细胞上的ETA受体）可能介导了前列腺素F2α的抑制作用。ET - 1与子宫前列腺素F2α激增同时出现的最高浓度这一观察结果也提示了ET - 1参与黄体退化。此外，给予前列腺素F2α可上调黄体中ET - 1的表达。黄体退化的后期阶段涉及程序性细胞死亡（PCD），可能由免疫细胞介导。ET - 1也可能通过促进白细胞迁移和刺激巨噬细胞释放肿瘤坏死因子α（TNFα）参与这一过程。黄体细胞（内皮细胞和类固醇生成细胞）上存在肿瘤坏死因子α受体1型（p55），它可引发PCD和黄体的结构破坏。
