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Abstract
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During mammalian spermatogenesis, the cytoskeleton system plays a significant role in morphological changes. The formation of abnormally shaped spermatozoa might be caused by a problem with the cytoskeleton system. Male infertility such as non-obstructive azoospermia (NOA) might be explained by studies of the cytoskeletal system during spermatogenesis.
The scaffold genes were analyzed by microarray and bioinformatics (300 sperm genes) and we used real time polymerase chain reaction for confirm these genes.
In the microarray analyses of three human cases with different NOA sperm, the expression of TBL3 (transducin beta like 3), MAGEA8 (MAGE family member A8) was upregulated, while expression of NTN1 (netrin 1) was downregulated. A combined analysis of Enrich Shiny Gene Ontology (GO), STRING, and Cytoscape was used to predict proteins' molecular interactions and then to recognize master pathways. Functional enrichment analysis showed that the biological process (BP) mitotic cytokinesis, cytoskeleton-dependent cytokinesis, positive regulation of stem cell proliferation, negative regulation of Rho protein signal transduction, supramolecular fiber organization, negative regulation of Ras protein signal transduction, positive regulation of protein localization to the cell periphery and positive regulation of cell-substrate adhesion were significantly expressed in up/ down regulated differentially expressed genes (DEGs) in sperm. In MF experiments of DEGs that were up/down regulated, it was found that GTPase and small GTPase bindings, tubulin bindings, gap junction channels, glutathione transmembrane transport, gap junction hemichannel activity, and tripeptide transmembrane transport were overexpressed. According to our findings, non-obstructive azoospermia and infertility can be explained by genes and their interacting hub proteins.
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