Differential cytoskeleton protein genes expression analysis between human sperm of patients with non-obstructive azoospermia and normal

Numerous research have recently focused on the function of cytoskeleton protein in spermatogenesis and male infertility. In the context of the etiopathogenesis of male infertility, we wanted to provide an overview of the information about the control of cytoskeleton protein gene during spermatogenesis. Overall, the results are consistent with the theory that sperm abnormalities and infertility are linked to sperm cytoskeleton protein. Differential methylation of a number of genes has been linked to poor spermatogenesis and/or reproductive failure. In order to identify the main pathways, the functional and molecular interactions of proteins were predicted using Enrich Shiny GO, STRING, and Cytoscape online assessments. This study has provided insight into the connection between cytoskeleton protein genes, including GOLGA۶L۶, CAPZA۱, CTNND۲, ACTR۳B, MYO۱۹ and KRT۳۵. The microarray analysis of six human cases with different non-obstructive azoospermia revealed that CTNND۲, ACTR۳B, MYO۱۹ and KRT۳۵ were up-regulated, and expression of GOLGA۶L۶ andCAPZA۱was down-regulated with the normal case. For this purpose, Enrich Shiny GO, STRING, and Cytoscape online evaluation was applied to predict proteins' functional and molecular interactions and then performed to recognize the master pathways. Enrich tool analysis revealed that the up-regulated DEGs were enriched in ۳ GO terms, while down-regulated DEGs were incorporated with ۳ GO terms. Enrich tool analysis revealed that the up-regulated DEGs were enriched in ۳ GO terms, while down-regulated DEGs were incorporated with ۳ GO terms. Functional enrichment analysis demonstrated that the biological process (BP) term “dendritic spine morphogenesis”, “peptidyl-lysine methylation” and “barbed-end actin filament capping” was significantly overexpressed in DEGs.Overrepresented molecular function (MF) terms in up-regulated DEGs included “plus-end-directed microtubule motor activity”, “myosin light chain binding” (myosin light chain binding), “microfilament motor activity” and “actin filament binding”. According to our research, these genes and the hub proteins that they interact with may contribute to understanding the pathophysiology of aberrant germ cells and infertility.