Mechanisms associated with corpus luteum development

Abstract

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.

Luteinization of porcine preovulatory follicles leads to systematic changes in follicular gene expression

“…The genes that had high expression in the preovulatory luteinized follicles fell into different functional categories when compared with preovulatory estrogenic follicles. The functional categories of genes that were highly expressed in preovulatory luteinized follicles were reminiscent of the cellular processes that have been classically ascribed to follicular cells after the LH surge (Smith et al 1994, Murphy et al 2001). …”

“…The release of the LH surge near the onset of estrus redirects preovulatory development and causes the biochemical differentiation of the follicle (luteinization) and ovulation (Richards et al 2002, Murdoch & Gottsch 2003. There is a shift from estrogen to progesterone synthesis, thinning and folding of the follicle wall, and dispersion of the granulosa cell layer (Smith et al 1994, Murphy et al 2001. Growth factors, proteases, and protease inhibitors coordinate tissue remodeling and angiogenesis that are essential for ovulation and the formation of the corpus luteum (Smith et al 2002, Tamanini & DeAmbrogi 2004.…”

“…Growth factors, proteases, and protease inhibitors coordinate tissue remodeling and angiogenesis that are essential for ovulation and the formation of the corpus luteum (Smith et al 2002, Tamanini & DeAmbrogi 2004. Perhaps, the most notable morphological change occurs within the microvasculature of the theca cell layer where there is hyperemia, edema, and extravagination of erythrocytes (Smith et al 1994, Murphy et al 2001.…”

KIT receptor-positive cells in the bovine corpus luteum are primarily theca-derived small luteal cells

“…An important process of developing mammalian CL is the ingrowth of capillary sprouts from the vascular thecal layer into the avascular granulosa layer (Smith et al 1994, Schams & Berisha 2004. Growing vessels are considered a vehicle for the dispersion of steroidogenic cells throughout the CL (Murphy et al 2001).…”

Induction of follicular luteinization by equine chorionic gonadotropin in cyclic guinea pigs

“…Like normal corpora lutea, the StAR and PCNA proteins were both expressed in luteinized follicles, with normal-level proliferation of luteinized cells. The active luteinized cells in the CL-like structure were believed to secrete progesterone like CL (Smith et al, 1994). CL-like structures (luteinized follicles from LUFs) can secrete progesterone (PlasRoser et al, 1984) and estrogen, which function differently from the corpora lutea (Westfahl, 1988).…”