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灵长类动物和反刍动物黄体调节的内分泌和细胞机制比较。

Comparison of endocrine and cellular mechanisms regulating the corpus luteum of primates and ruminants.

作者信息

Wiltbank M C, Salih S M, Atli M O, Luo W, Bormann C L, Ottobre J S, Vezina C M, Mehta V, Diaz F J, Tsai S J, Sartori R

机构信息

Department of Dairy Science, University of Wisconsin-Madison, WI, USA ; Department of Animal Sciences, ESALQ, University of Sao Paulo, Piracicaba, Brazil.

出版信息

Anim Reprod. 2012 Jul;9(3):242-259.

Abstract

The corpus luteum (CL) is a transient endocrine organ that is essential for maintenance of pregnancy in both ruminants and primates. The cellular and endocrine mechanisms that regulate the CL in these species have commonalities and some distinct and intriguing differences. Both species have similar cellular content with large luteal cells derived from the granulosa cells of the follicle, small luteal cells from follicular thecal cells, and large numbers of capillary endothelial cells that form the vasculature that has an essential role in optimal CL function. Intriguingly, the large luteal cells in ruminants grow larger than in primates and acquire a capacity for high constitutive progesterone (P4) production that is independent of stimulation from LH. In contrast, the primate CL and the granulosa lutein cells from primates continue to require stimulation by LH/CG throughout the luteal phase. Although the preovulatory follicle of women and cows had similar size and steroidogenic output (10 to 20 mg/h), the bovine CL had about ten-fold greater P4 output compared to the human CL (17.4 1.4 mg/h), possibly due to the development of high constitutive P4 output by the bovine large luteal cells. The continued dependence of the primate CL on LH/CG/cAMP also seems to underlie luteolysis, as there seems to be a requirement for greater luteotropic support in the older primate CL than is provided by the endogenous LH pulses. Conversely, regression of the ruminant CL is initiated by PGF from the nonpregnant uterus. Consequently, the short luteal phase in ruminants is primarily due to premature secretion of PGF by the nonpregnant uterus and early CL regression, whereas CL insufficiency in primates is related to inadequate luteotropic support and premature CL regression. Thus, the key functions of the CL, pregnancy maintenance and CL regression in the absence of pregnancy, are produced by common cellular and enzymatic pathways regulated by very distinct luteotropic and luteolytic mechanisms in the CL of primates and ruminants.

摘要

黄体(CL)是一种临时性内分泌器官,对反刍动物和灵长类动物维持妊娠至关重要。在这些物种中调节黄体的细胞和内分泌机制既有共性,也存在一些独特且有趣的差异。两种物种的细胞成分相似,大型黄体细胞源自卵泡的颗粒细胞,小型黄体细胞来自卵泡膜细胞,还有大量的毛细血管内皮细胞形成血管系统,该系统对黄体的最佳功能起着至关重要的作用。有趣的是,反刍动物的大型黄体细胞比灵长类动物的更大,并且具有独立于促黄体生成素(LH)刺激产生高基础孕酮(P4)的能力。相比之下,灵长类动物的黄体和颗粒黄体细胞在整个黄体期都持续需要LH/CG的刺激。尽管女性和奶牛的排卵前卵泡大小和类固醇生成量相似(10至20毫克/小时),但与人类黄体(17.4±1.4毫克/小时)相比,牛黄体的P4产量大约高十倍,这可能是由于牛大型黄体细胞高基础P4产量的发展。灵长类动物黄体对LH/CG/cAMP的持续依赖似乎也是黄体溶解的基础,因为老年灵长类动物黄体似乎比内源性LH脉冲提供的促黄体支持需要更多。相反,反刍动物黄体的退化是由未孕子宫分泌的前列腺素F(PGF)引发的。因此,反刍动物黄体期短主要是由于未孕子宫过早分泌PGF和黄体过早退化,而灵长类动物黄体功能不全与促黄体支持不足和黄体过早退化有关。因此,黄体的关键功能,即维持妊娠和在未妊娠时黄体退化,是由灵长类动物和反刍动物黄体中非常不同的促黄体和溶黄体机制调节的共同细胞和酶途径产生的。

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