Abstract
Follicle stimulating hormone (FSH) is produced by the pituitary gland in a coordinated hypothalamic–pituitary–gonadal (HPG) axis event, plays important roles in reproduction and germ cell development during different phases of reproductive development (fetal, neonatal, puberty, and adult life), and is consequently essential for fertility. FSH is a heterodimeric glycoprotein hormone of two dissociable subunits, α and β. The FSH β-subunit (FSHβ) function starts upon coupling to its specific receptor: follicle-stimulating hormone receptor (FSHR). FSHRs are localized mainly on the surface of target cells on the testis and ovary (granulosa and Sertoli cells) and have recently been found in testicular stem cells and extra-gonadal tissue. Several reproduction disorders are associated with absent or low FSH secretion, with mutation of the FSH β-subunit or the FSH receptor, and/or its signaling pathways. However, the influence of FSH on germ cells is still poorly understood; some studies have suggested that this hormone also plays a determinant role in the self-renewal of germinative cells and acts to increase undifferentiated spermatogonia proliferation. In addition, in vitro, together with other factors, it assists the process of differentiation of primordial germ cells (PGCLCs) into gametes (oocyte-like and SSCLCs). In this review, we describe relevant research on the influence of FSH on spermatogenesis and folliculogenesis, mainly in the germ cell of humans and other species. The possible roles of FSH in germ cell generation in vitro are also presented.
Highlights
Introduction published maps and institutional affilFollicle stimulating hormone (FSH) and luteinizing hormone (LH) are gonadotropins essential for proper reproduction and fertility in both females and males; they are key players in germ cell formation [1,2]
Gametogenesis starts after the primordial germ cells (PGCs) co addition, we present the use of FSH in the induction of germ cells and germ-cell-like cells the migration process to the gonadal ridge
FSH controls the proliferation of Sertoli cells by activating cyclic adenosine monophosphate/protein kinase A mitogen-activated protein kinase (ERK1/2), and phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase B (PKB/AKT)/mechanistic target of rapamycin pathways, and increasing the transcription of c-Myc, hypoxiainducible factor 2 alpha (HIF2), and cyclin D1 (CCND1) [112,114,115]
Summary
Fetal and Neonatal Periods pigs, ~E25–30 days for cows, and ~4 weeks for humans) [72,73,74,75]. Studies have reported that XX males of different species (human, dog, mouse, and other mammals) who lack SRY present the male phenotype with normal Sertoli cells, suggesting that activation of other factors and the expression of genes such as SOX9 are important for sex differentiation [81,82,83,84]. The SOX9 gene is not on the Y chromosome, but is expressed in males in most vertebrates, unlike SRY, which is found only in mammals [81] In domestic animals such as pigs, morphological gonadal differentiation starts at 28 days of gestation, and complete differentiation is observed at 30–35 days of gestation (unpublished data [85]), at the fifth to sixth week in humans, and between E10.5 and. FSH controls the proliferation of Sertoli cells by activating cyclic adenosine monophosphate/protein kinase A (cAMP/PKA) mitogen-activated protein kinase (ERK1/2), and phosphatidylinositol 3-kinase (PI3K)/serine/threonine protein kinase B (PKB/AKT)/mechanistic target of rapamycin (mTORC1) pathways, and increasing the transcription of c-Myc, hypoxiainducible factor 2 alpha (HIF2), and cyclin D1 (CCND1) [112,114,115]
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