Abstract
The Importance and key role of Wnt/β-catenin signaling pathway in spermatogenesis is known. Abnormalities of this pathway in Sertoli and germ cells leads to infertility. Leydig cells play an important role in spermatogenesis and male reproduction. As of now, exact position of the Wnt/β-catenin signaling pathway disorders in the tissue and possible involvement of Leydig cells has not been investigated. Samples of our previous study were used for common Y chromosome microdeletions screening and common CFTR gene mutations.1 β-catenin gene expression were evaluated and compared between testicular tissue obtained by testicular sperm extraction (TESE) in two groups of obstructive (n=10) and non-obstructive (n=10) azoospermic infertile men. Location of β-catenin accumulation was detected by immunofluorescence technic and quantitatively compared in the tissue followed by counterstaining with anti-vimentin antibody. It was used as specific marker of leydig cells to determine and confirm the cells in which this gathering was occurred. β-catenin gene expression does not have a significant difference between the obstructive azoospermia (0.998) and non-obstructive azoospermia group (0.891). β-catenin was abnormally aggregated in leydig cell of non-obstructive azoospermic men. Gathering β-catenin in cytoplasm of leydig cells can disrupt spermatogenesis and cause infertility in men.
Highlights
Male sex hormone testosterone is made by leydig cells in the interstitial tissue of the testes form about 20 percent of the adult testes weight
Samples of our previous study were used for common Y chromosome microdeletions screening and common CFTR gene mutations.[1] β-catenin gene expression were evaluated and compared between testicular tissue obtained by testicular sperm extraction (TESE) in two groups of obstructive (n=10) and non-obstructive (n=10) azoospermic infertile men
Results: β-catenin gene expression does not have a significant difference between the obstructive azoospermia (0.998) and non-obstructive azoospermia group (0.891). β-catenin was abnormally aggregated in leydig cell of non-obstructive azoospermic men
Summary
Male sex hormone testosterone is made by leydig cells in the interstitial tissue of the testes form about 20 percent of the adult testes weight. In the absence of activating Wnt signal, β-catenin is phosphorylated by GSK3-β-Axin (a cell scaffold protein)-APC (Adenomatous polyposis coli) complex It is ubiquinated and degraded by proteasome. This chain reaction causes repression of target gene.[4,5,6,7] Noncanonical pathway acts through alternative molecules other than β-catenin.[8] Several types of Wnt proteins including 1, 3, 4, 5a and 7a in the testes of fetal and adult rodents and humans have been reported.[9,10,11,12,13] Some components of the Wnt/βcatenin signaling pathway such as Fz9, Nkd[1] and βcatenin have been identified in the testis.[14] β-catenin has a high level expression in mice germ and sertoli cells.[15] Impaired β-catenin signaling in Sertoli cells of the mouse embryo results in the destruction of the testicular cord and Mullerian duct.[16] The aberrant activity of Wnt/βcatenin signaling pathway leads to abnormal differentiation of the PGCs.[17] Wnt/β-catenin signaling pathway and androgen receptors have direct effect each other in many aspects. This study was aimed to investigate the probability of disruption of Wnt/β-catenin signaling pathway in leydig cells of azoospermic men
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