Abstract
The follicle-stimulating hormone receptor (FSH-R) expression was always considered human gonad-specific. The receptor has also been newly detected in extragonadal tissues. In this finding, we evaluated FSH-R expression in the human male early genital tract, in testicular tumors, and in sperm from healthy and varicocele patients. In sperm, we also studied the mechanism of FSH-R action. Immunohystochemistry and Western blot analysis showed FSH-R presence in the first pathways of the human genital tract, in embryonal carcinoma, and in sperm, but it was absent in seminoma and in lower varicocele. In sperm, FSH/FSH-R activity is mediated by G proteins activating the PKA pathway, as we observed by using the H89. It emerged that increasing FSH treatments induced motility, survival, capacitation, and acrosome reaction in both sperm samples. The different FSH-R expression in tumor testicular tissues may be discriminate by tumor histological type. In spermatozoa, FSH-R indicates a direct action of FSH in these cells, which could be beneficial during semen preparation for in vitro fertilization procedures. For instance, FSH positive effects could be relevant in idiopathic infertility and in the clinic surgery of varicocele. In conclusion, FSH-R expression may be considered a molecular marker of testicular disorders.
Highlights
The follicle-stimulating hormone (FSH), a central hormone of mammalian reproduction, is produced by the gonadotroph cells in the anterior pituitary gland and the classical target organs are the ovary and testis [1,2].In recent years, follicle-stimulating hormone receptor (FSH-R) has been detected in extragonadal sites, including bone, monocytes, different sites of the female reproductive tract, and the liver [3,4,5,6,7,8,9]
FSH-R has been detected in extragonadal sites, including bone, monocytes, different sites of the female reproductive tract, and the liver [3,4,5,6,7,8,9]
Bovine serum albumin (BSA) protein standard, Laemmli sample buffer, pre-stained molecular weight markers, haematoxylin, eosin Y, dimethylsulfoxide (DMSO), Earle’s balanced salt solution (EBSS), and all other chemicals were purchased from Sigma-Aldrich (Milan, Italy)
Summary
The follicle-stimulating hormone (FSH), a central hormone of mammalian reproduction, is produced by the gonadotroph cells in the anterior pituitary gland and the classical target organs are the ovary and testis [1,2]. FSH-R has been detected in extragonadal sites, including bone, monocytes, different sites of the female reproductive tract, and the liver [3,4,5,6,7,8,9]. All the reports point to Sertoli cells as the exclusive FSH target in the testis, the sites of FSH action within the human male reproductive system are not resolved yet. Since FSH-R possesses several polymorphisms able to affect receptor sensitivity and expression [10,11], the attention on this. Life 2020, 10, 336 receptor has been always paid based on these issues. From several gene knockout experiments on FSH and FSH-R, it emerged that FSH-deficient male mice had small testes [12] and that FSH-R mutations are associated with variable degrees of spermatogenic failure [13]
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