The hormone secretion pattern of the corpus luteum difers from that of the follicle (see Fig. 5-1). As depicted in Figure 5-2, the greater capacity of granulosa-lutein cells to produce progesterone results from enhanced access to considerably more steroidogenic precursors through blood-borne, low-densiry lipoprotein (LDL)-derived cholesterol (Carr, 1981a). Ovarian progesterone production peaks at 25 to 50 mg/d during the midluteal phase. With pregnancy, the corpus luteum continues progesterone production in response to placental human chorionic gonadotropin (hCG), which binds to the same receptor as LH.
Estrogen levels follow a more complex pattern of secretion.
Specifically, just after ovulation, estrogen levels decline, but then exhibit a secondary rise that reaches a peak production of 0.25 mg/d of 173-estradiol in the midluteal phase. Toward the end of the luteal phase, estradiol production again drops.
The human corpus luteum is a transient endocrine organ that, in the absence of pregnancy, will rapidly regress 9 to 11 days after ovulation via apoptosis (Vaskivuo, 2002). The mechanisms that control luteolysis, that is, the regression of the corpus luteum, remain unclear. However, it results in part from dropping levels of circulating LH in the late luteal phase and rising LH insensitivity by luteal cells (Duncan, 1996; Filicori, 1986). he role of other factors is less established. The dramatic drop in circulating estradiol and progesterone levels initiate molecular events that lead to menstruation.
Estrogen is the essential hormonal signal on which most events in the normal menstrual cycle depend. They function in many cell types to regulate follicular development, uterine receptivity, and blood flow. The most biologically potent naturally occur ring estrogen is 173-estradiol, which is secreted by granulosa cells of the dominant follicle and luteinized granulosa cells of the corpus luteum. Estradiol action is complex and appears estrogen receptor a (ERa) and 3 (ER3) (Katzen ellenbogen, 2001). These isoforms are the products of separate genes and can exhibit distinct tissue expression. Both estradiol-receptor complexes act as transcriptional factors that become associ ated with the estrogen-response element of speciic genes. They share a robust activation by estradiol. However, diferences in their binding ainities to other estrogens and their cell-speciic may have both distinct and overlapping function (Saunders, 2005).
Most progesterone actions on the female reproductive tract are mediated through the nuclear hormone receptors, progesterone-receptor type A (PR-A) and B (PR-B). Progesterone enters cells by difusion, and in responsive tissues it becomes associated with its receptors (Conneely, 2002). Progesteronereceptor isoforms arise from a single gene and regulate transcription of target genes. hese receptors have unique actions. When PR-A and PR-B receptors are coexpressed, it appears that PR-A can inhibit PR-B gene regulation. The endometrial glands and stroma appear to have diferent expression patterns for progesterone receptors that vary during the menstrual cycle (Mote, 1999).
Progesterone can also evoke rapid responses, such as changes in intracellular free calcium levels, which cannot be explained by genomic mechanisms. G-protein-coupled membrane receptors for progesterone have been identiied, but their role in the ovarian-endometrial cycle remains to be elucidated (Peluso, 2007).