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Changes in Sertoli Cell Structure and Function
Published in Tom O. Abney, Brooks A. Keel, The Cryptorchid Testis, 2020
David M. de Kretser, Gail P. Risbridger
Androgen-binding protein is a specific and well-defined product of the Sertoli cell.29,30 The precise physiological role of ABP is unclear, but it has been suggested that it acts as a carrier of androgens within the Sertoli cell itself, or from the testis to the epididymis.2 ABP produced by the Sertoli cell is secreted with seminiferous tubule fluid into the lumen and is transported to the duct system of the epididymis where it is taken up by the epithelial cells of the proximal caput region, or secreted into seminal fluid at ejaculation. ABP is also released from the basal surface of the Sertoli cell, is present in testicular fluid, and can be detected in serum or plasma. Thus, the secretion of ABP from the Sertoli cells is bidirectional, although the greater proportion of ABP is released at the luminal aspect of the Sertoli cell. The production of ABP by the Sertoli cell ceases after hypophysectomy but can be restored after treatment with pituitary hormones (LH and FSH).24,31,32
Hormonal regulation of spermatogenesis
Published in Rajender Singh, Molecular Signaling in Spermatogenesis and Male Infertility, 2019
Pallav Sengupta, Mohamed Arafa, Haitham Elbardisi
The hypothalo-pituitary-gonadal (HPG) axis holds prime control over the process of spermatogenesis. The hypothalamus induces gonatropin secretion from the anterior pituitary by the pulsatile release of gonadotropin-releasing hormone (GnRH) (2,3). Uninterrupted proper spermatogenesis is maintained through steady high intratesticular testosterone. Testosterone production is induced by the gonadotropin, luteinizing hormone (LH)–stimulated Leydig cells. Testosterone crosses the tubular basement membrane and diffuses into the Sertoli cells to bind with androgen binding protein (ABP) (4,5). Sertoli cells also possess receptors for follicle-stimulating hormone (FSH) that are probably required for the initiation of spermatogenesis (6,7). Sertoli cells also produce glycoprotein hormones such as inhibins, activins and follistatin that mediate feedback regulations of the principal hormones. Apart from the classical hormones, there are several metabolic hormones, growth factors as well as paracrine factors that influence spermatogenesis either via their direct effect on the testicular cells or by affecting the hormonal cross-talks (8). This chapter presents an easy understanding of the complex hormonal regulations of spermatogenesis.
Changes in Gene Expression During Aging of Mammals
Published in Alvaro Macieira-Coelho, Molecular Basis of Aging, 2017
The age-dependent expression of the α2μ-globulin gene correlates well with the appearance and disappearance of cytoplasmic androgen-binding protein (AR) in the liver. AR is absent before day 40, and disappears after about day 800. It was shown that its gene becomes sensitive to DNAase I after about day 20 and retains the sensitivity for the rest of the life span.19 The gene is not expressed after about day 900. Hence DNAase I sensitivity is not the only requirement for its expression.
The effects of long-term testosterone treatment on endocrine parameters in hypogonadal men: 12-year data from a prospective controlled registry study
Published in The Aging Male, 2022
Aksam Yassin, Farid Saad, Mustafa Alwani, Omar M. Aboumarzouk, Raed M. Al-Zoubi, Joanne Nettleship, Daniel Kelly, Abdulla Al-Ansari
Whilst prolactin receptors are present in the male reproductive organs, the exact role of this hormone in male reproductive physiology remains unclear [50]. The secretion of GnRH by the hypothalamus is pulsatile in nature and triggers LH and consequently T synthesis. Prolactin inhibits this pulsatile secretion of GnRH and therefore the release of LH and T. Serum prolactin did not alter during the study period and remained within the reference range of 2–18ng/mL for males [51]. This is of importance as even mild to moderate increases in serum prolactin, if chronic, may negatively affect spermatogenesis and fertility as suggested by studies in adult rats [52]. This effect on fertility may be due to its participation in the HPT axis described above [53], or via reduction in androgen-binding protein expression which is a paracrine regulator of spermatogenesis as described by Aleem et al. [52].
Repeated administrations of Mn3O4 nanoparticles cause testis damage and fertility decrease through PPAR-signaling pathway
Published in Nanotoxicology, 2020
Xiao Zhang, Zongkai Yue, Haijun Zhang, Lu Liu, Xiaomeng Zhou
It is well known that spermatozoa are produced from spermatogonial stem cells by a series of process involving mitosis, meiosis and cellular differentiation, and spermatogenesis is essential for sexual reproduction (Oliva and Castillo 2011). Meanwhile, spermatogenesis process is subjected to the neuroendocrine hypothalamic-pituitary-gonadal (HPG) axis (Huleihel and Lunenfeld 2004). In addition, hormones secreted by hypothalamus are transported to the pituitary gland via the blood and then induce the production and secretion of gonadotropins which in turn are transported to testes by the blood (Kong et al. 2014). LH stimulates the Leydig cells in the testes to synthesize and secrete the testosterone (Li et al. 2013). FSH and T stimulate Sertoli cells to produce androgen binding protein and improve the formation of the BTB, meanwhile, FSH and T could support and nourish the sperm cells during their maturation (Sofikitis et al. 2008). In this study, the serum T, FSH, and LH levels in serum of rats were determined to investigate the effect of Mn3O4-NPs on sex hormones. The serum T and FSH levels were significantly decreased in Mn3O4-NPs-120 d compared with those in the Mn3O4-NPs-0 d and Mn3O4-NPs-60 d, indicating that the serum T and FSH were suppressed in a time-dependent manner after administrated with Mn3O4-NPs. All results suggest that Mn3O4-NPs can disturb the normal HPG axis function which correlated with the malfunction in spermatogenesis and male infertility.
The use of platelet-rich plasma (PRP) to improve structural impairment of rat testis induced by busulfan
Published in Platelets, 2019
Farzaneh Dehghani, Narges Sotoude, Hossein Bordbar, M.R. Panjeshahin, Saied Karbalay-Doust
Since infertility is a major problem in society, different treatment modalities have been recommended. Recently, the use of growth factors to treat infertility has been considered. Previous researches have showed that germ cells produce vascular endothelial growth factor (VEGF) that is essential for survival of spermatogonia stem cells (7). Bone morphogenic protein-4 (BMP-4) has an important role in the proliferation and differentiation of germ cells (8). Insulin growth factor-1(IGF-1) is a mitogen agent that has a positive effect on spermatogenesis/steroidogenesis (9). Epidermal growth factor (EGF) has a beneficial effect on spermatogenesis (10). Studies have also shown that fibroblast growth factor (FGF) and EGF stimulate the Sertoli cell to androgen-binding protein, transferrin, and inhibit secretion (11). Platelet-derived growth factor (PDGF) has a positive effect on the germinal cells and autocrine/paracrine function regulation. These growth factors reduce the tissue ischemic of the testes, improve seminal-producing tubules diameter, the maintenance of germinal epithelium, as well as regulating Leydig and Sertoli cells function (12–15). It seems that the combination of these growth factors might have a positive effect on spermatogenesis and fertility.