Abstract
Gonadotropins are essential for regulating ovarian development, steroidogenesis, and gametogenesis. While follicle stimulating hormone (FSH) promotes the development of ovarian follicles, luteinizing hormone (LH) regulates preovulatory maturation of oocytes, ovulation, and formation of corpus luteum. Cognate receptors of FSH and LH are G-protein coupled receptors that predominantly signal through cAMP-dependent and cAMP-independent mechanisms that activate protein kinases. Subsequent vital steps in response to gonadotropins are mediated through activation or inhibition of transcription factors required for follicular gene expression. Estrogen receptors, classical ligand-activated transcriptional regulators, play crucial roles in regulating gonadotropin secretion from the hypothalamic–pituitary axis as well as gonadotropin function in the target organs. In this review, we discuss the role of estrogen receptor β (ERβ) regulating gonadotropin response during folliculogenesis. Ovarian follicles in Erβ knockout (ErβKO) mutant female mice and rats cannot develop beyond the antral state, lack oocyte maturation, and fail to ovulate. Theca cells (TCs) in ovarian follicles express LH receptor, whereas granulosa cells (GCs) express both FSH receptor (FSHR) and LH receptor (LHCGR). As oocytes do not express the gonadotropin receptors, the somatic cells play a crucial role during gonadotropin induced oocyte maturation. Somatic cells also express high levels of estrogen receptors; while TCs express ERα and are involved in steroidogenesis, GCs express ERβ and are involved in both steroidogenesis and folliculogenesis. GCs are the primary site of ERβ-regulated gene expression. We observed that a subset of gonadotropin-induced genes in GCs, which are essential for ovarian follicle development, oocyte maturation and ovulation, are dependent on ERβ. Thus, ERβ plays a vital role in regulating the gonadotropin responses in ovary.
Highlights
Follicle stimulating hormone (FSH) and luteinizing hormone (LH) are called gonadotropins due to their effects on gonadal development and function [1,2] Gonadotropins are secreted from the anterior pituitary gland and act on the ovary and testis [1,2]
Gonadotropins interact with intraovarian factors to regulate steroidogenesis, follicle development, oocyte maturation, ovulation, and formation of the corpus luteum [1,2,3,4,5] Estrogens synthesized in the ovary during folliculogenesis in turn act on the hypothalamic– pituitary (H–P) axis to regulate gonadotropin secretion [2]
LH signaling in theca cells (TCs) plays an essential role in initiating steroidogenesis, whereas LH binding to LH/chorionic gonadotropin (CG) receptor (LHCGR) induces differentiation of granulosa cells (GCs), which is required for cumulus expansion, oocyte maturation, ovulation, and luteinization [6,93]
Summary
Follicle stimulating hormone (FSH) and luteinizing hormone (LH) are called gonadotropins due to their effects on gonadal development and function [1,2] Gonadotropins are secreted from the anterior pituitary gland and act on the ovary and testis [1,2]. Gonadotropins interact with intraovarian factors to regulate steroidogenesis, follicle development, oocyte maturation, ovulation, and formation of the corpus luteum [1,2,3,4,5] Estrogens synthesized in the ovary during folliculogenesis in turn act on the hypothalamic– pituitary (H–P) axis to regulate gonadotropin secretion [2]. Ovarian follicles consist of oocytes surrounded by two types of somatic cells, granulosa cells (GCs) and theca cells (TCs). These somatic cells are involved in steroidogenesis, and regulation of oocyte development from the dormant stage to ovulation. Gonadotropin response that leads to oocyte maturation is mediated through the signaling within somatic cells [6]. We discuss the role of ERβ in regulating the gonadotropin responses in ovaries
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