Smith M F, McIntush E W, Smith G W
Department of Animal Sciences, University of Missouri, Columbia 65211.
J Anim Sci. 1994 Jul;72(7):1857-72. doi: 10.2527/1994.7271857x.
The transition of a preovulatory follicle into a corpus luteum is a complex process involving mechanisms similar to wound healing and tumor formation. The objective of this review is to focus on mechanisms associated with corpus luteum development with specific attention to the follicular lineage of luteal cells, mechanisms associated with luteinization, and neovascular changes during luteal development. Corpora lutea are a continuation of follicular maturation and form from granulosal and theca interna cells. There is morphological and immunological evidence in ruminant species for the differentiation of granulosal and theca interna cells into large and small steroidogenic luteal cells, respectively. Different morphological, physiological, and biochemical characteristics of large and small luteal cells may reflect different follicular lineages with separate embryological origins. Following the preovulatory gonadotropin surge, follicular cells begin morphological, endocrinological, and biochemical changes associated with luteinization. Luteinization involves the transition of a preovulatory follicle into a highly vascular corpus luteum capable of secreting large quantities of progesterone. In addition, various cell types undergo hyperplasia, hypertrophy, and(or) migration during corpus luteum formation. An essential component of corpus luteum development is the recruitment of a blood supply. The development of a new microcirculatory bed involves breakdown of the follicular basement membrane, endothelial cell migration, endothelial cell proliferation, and development of capillary lumina. This process is regulated by the interaction of angiogenic and antiangiogenic substances. Further clarification of the preceding mechanisms may result in the development of improved methodologies for controlling the time of ovulation and(or) increasing pregnancy rates.
排卵前卵泡向黄体的转变是一个复杂的过程，涉及与伤口愈合和肿瘤形成相似的机制。本综述的目的是聚焦于与黄体发育相关的机制，特别关注黄体细胞的卵泡谱系、与黄体化相关的机制以及黄体发育过程中的新生血管变化。黄体是卵泡成熟的延续，由颗粒细胞和卵泡内膜细胞形成。在反刍动物中，有形态学和免疫学证据表明颗粒细胞和卵泡内膜细胞分别分化为大、小类固醇生成黄体细胞。大、小黄体细胞不同的形态、生理和生化特征可能反映了具有不同胚胎学起源的不同卵泡谱系。排卵前促性腺激素高峰后，卵泡细胞开始发生与黄体化相关的形态、内分泌和生化变化。黄体化涉及排卵前卵泡向能够分泌大量孕酮的高度血管化黄体的转变。此外，在黄体形成过程中，各种细胞类型会发生增生、肥大和（或）迁移。黄体发育的一个重要组成部分是血供的募集。新的微循环床的发育涉及卵泡基底膜的破坏、内皮细胞迁移、内皮细胞增殖以及毛细血管腔的形成。这个过程受血管生成和抗血管生成物质相互作用的调节。对上述机制的进一步阐明可能会带来改进的方法，用于控制排卵时间和（或）提高妊娠率。
