The primary androgen produced by thecal cells, which express LH receptors, is primarily androstenedione. Steroidogenic enzymes are stimulated by basal levels of LH in thecal cells. Thecal cells have access to cholesterol within LDL and HDL lipoprotein particles because they are richly vascularized. The import of cholesterol is facilitated by LH promoting the expression of the LDL receptor and HDL receptor (SR-B1). LH also promotes the expression of CYP11A1, 3β-HSD, and CYP17, which have side chain cleavage enzyme, 17-hydroxylase activity, and 17,20-lyase activity, respectively. Androgens, primarily androstenedione but also some testosterone, are released from the theca and diffuse into the mural granulosa cells or enter the vasculature surrounding the follicle.

The mural granulosa cells of the selected follicle have a high number of FSH receptors and are very sensitive to FSH. FSH upregulates the gene expression and activity of CYP19 (aromatase). CYP19 converts androstenedione to the weak estrogen estrone and converts testosterone to the potent estrogen estradiol-17β. Granulosa cells also express activating isoforms of 17β-HSD, which converts estrone to highly active estradiol-17β. Additionally, FSH induces the expression of inhibin B during the follicular phase.

During the second half of the follicular phase, FSH induces the expression of LH receptors in mural granulosa cells. This allows these cells to maintain high levels of CYP19 despite declining FSH levels. The acquisition of LH receptors also ensures that mural granulosa cells respond to the LH surge.

The periovulatory period, which lasts for 32 to 36 hours in women, is defined as the time from the onset of the LH surge to ovulation. During this period, there is a change in the steroidogenic function of theca and mural granulosa cells, known as luteinization. This leads to the formation of a corpus luteum that produces high amounts of progesterone and estrogen within a few days after ovulation. The LH surge induces the onset of complex processes that complete the gametogenic function of the ovary for the month and prepares the female reproductive tract for implantation and gestation.

The LH surge induces structural changes in the dominant follicle, including its rupture, ovulation of the cumulus-oocyte complex, and the formation of the corpus luteum from the remaining thecal and mural granulosa cells. Major structural changes occur during this transition. Before ovulation, the large preovulatory follicle presses against the ovarian surface, creating a poorly vascularized bulge called the stigma. The LH surge triggers the release of inflammatory cytokines and hydrolytic enzymes from the theca and granulosa cells. These secreted components cause the breakdown of the follicle wall, tunica albuginea, and surface epithelium near the stigma. As a result, the antral cavity becomes continuous with the peritoneal cavity.
Fig. 44.20, T ) express LH receptors and produce primarily androstenedione. Basal levels of LH stimulate expression of steroidogenic enzymes in thecal cells. The thecal cells are richly vascularized and thus have access to cholesterol within the lipoprotein articles LDL and HDL. LH promotes expression of the LDL receptor and HDL receptor (SR-B1), which import cholesterol. LH also promotes robust expression of CYP11A1 (side chain cleavage enzyme), 3β-HSD, and CYP17 with both 17-hydroxylase activity and 17,20-lyase activity. Androgens (primarily androstenedione but also some testosterone) released from the theca diffuse into the mural granulosa cells or enter the vasculature surrounding the follicle.
The mural granulosa cells (see
Fig. 44.20, MG) of the selected follicle have a high number of FSH receptors and are very sensitive to FSH, which upregulates CYP19 (aromatase) gene expression and activity. CYP19 converts androstenedione to the weak estrogen estrone and converts testosterone to the potent estrogen estradiol-17β. Granulosa cells express activating isoforms of 17β-HSD, which converts the less active estrone to highly active estradiol17β. In addition, FSH induces expression of inhibin B during the follicular phase.
Importantly, FSH also induces expression of LH receptors in mural granulosa cells during the second half of the follicular phase (see
Fig. 44.20). Thus mural granulosa cells acquire the ability to respond to LH, which allows these cells to maintain high levels of CYP19 in the face of declining FSH levels. Acquisition of LH receptors also ensures that mural granulosa cells respond to the LH surge.
The Dominant Follicle During the Periovulatory Period
The periovulatory period is defined as the time from the onset of the LH surge to expulsion of the cumulus-oocyte complex out of the ovary (i.e., ovulation). This process lasts for 32 to 36 hours in women. Starting at the same time and superimposed on the process of ovulation is a change in the steroidogenic function of theca and mural granulosa cells. This process is called luteinization and culminates in formation of a corpus luteum that is capable of producing high amounts of progesterone, along with estrogen, within a few days after ovulation. Thus the LH surge induces the onset of complex processes during the periovulatory period that complete the gametogenic function of the ovary for a given month and switches the endocrine function to prepare the female reproductive tract for implantation and gestation.
The LH surge induces dramatic structural changes in the dominant follicle that involves its rupture, ovulation of the cumulus-oocyte complex, and biogenesis of a new structure called the corpus luteum from the remaining thecal and mural granulosa cells. Major structural changes occur during this transition: 1. Before ovulation the large preovulatory follicle presses against the ovarian surface and generates a poorly vascularized bulge of the ovarian wall called the stigma. The LH surge induces release of inflammatory cytokines and hydrolytic enzymes from the theca and granulosa cells. These secreted components lead to breakdown of the follicle wall, tunica albuginea, and surface epithelium in the vicinity of the stigma (
Fig. 44.21 ). At the end of this process the antral cavity becomes continuous with the peritoneal cavity.