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Gonadotropins in the Female
Published in Paul V. Malven, Mammalian Neuroendocrinology, 2019
Figure 12-1 illustrates the complex actions of LH and FSH on theca interna and granulosa cells of ovarian follicles that result eventually in the secretion of estradiol into blood. As is true for other hormonal peptides, the action of LH or FSH depends on the target cells possessing cell-surface receptors specific for one of these blood-borne gonadotrophic hormones. The ovarian secretion of estradiol is very complex because the receptors differ among cell types and also vary with the degree of gonadotrophic stimulation of follicular growth. The wall of the follicle consists of an inner non-vascularized layer of granulosa cells that line the follicle wall and surround the oocyte. This inner layer of granulosa cells, also called membrana granulosa, is separated from the vascularized layer of theca interna cells by the basement membrane of the follicle. The cells of the membrana granulosa are not a homogeneous population probably due to location-dependent specializations. Granulosa cells located in the cumulus region surrounding the oocyte appear to have specialized contacts with the oocyte. The layers of granulosa cells located just inside the basement membrane are classified as pseudostratified because processes from the cells in several layers have contact with the basement membrane (Lipner and Cross, 1968). However, some granulosa cells located in the interior of the follicle lack cellular contact with the basement membrane.
The effects of the anti-Müllerian hormone on folliculogenesis in rats: light and electron microscopic evaluation
Published in Ultrastructural Pathology, 2021
Premature luteinization was interesting in some growing follicles in AMH applied experimental groups. Ultrastructural changes characterized with increased lipid droplets, mitochondria with tubular cristae, and presence of agranular endoplasmic reticulum cisternae in granulosa cells of some preantral follicles were similar to the features after ovulation. Oktem O and Urman B reported that growth factors derived from the oocyte, like BMP-6, BMP-15, and GDF-9, prevent premature luteinization till the ovulation.3 Premature luteinization findings in AMH applied groups show that AMH may affect the mechanisms that prevent premature luteinization. Premature luteinization may be a result of impaired secretion of BMP-6, BMP-15, and GDF-9 from the oocyte or inhibition of FSH receptors on granulosa cells by AMH, so that granulosa cells underwent premature luteinization. Inhibitory effects of AMH on the expression of steroidogenic acute regulatory protein, aromatase activity, and luteinizing hormone receptor expression could be the reason for premature luteinization and increased concentrations of progesterone in experimental groups, even though the serum LH concentrations were similar between the experimental and control groups. Excess androgen in PCOS may be the reason for oocyte loss and results in premature luteinization by the decline in inhibitory paracrine factors secreted from oocytes.35 Although the way of early luteinization that has caused by AMH could be a subject of further studies, early luteinization will affect follicle development negatively and will result in anovulation in these follicles. Cystic, but not atretic, follicles were seen in all AMH-applied groups; ultrastructural findings of cystic follicles coincided with the reports of Manneas et al. who studied experimentally created PCOS.36 Okutsu et al. suggested that exogenous androstenedione induces cystic follicle formation; apoptosis of granulosa cells that face with the antral cavity results in membrana granulosa layer attenuation, consequently cystic follicles develop.35 They also reported increased lipid droplets in cytoplasms of granulosa cells in cystic follicles.35 Attenuated membrana granulosa layer and the presence of lipid droplets in granulosa cells support us that these follicles had become cystic.