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Identification of key genes in type 2 diabetes‐induced erectile dysfunction rats with stem cell therapy through high‐throughput sequencing and bioinformatic analysis
Author(s) -
Kang JiaQi,
Song YuXuan,
Liu Li,
Lu Yi,
Tian Jia,
Hu Rui,
Wang Xiao,
Liu XiaoQiang
Publication year - 2021
Publication title -
andrologia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.633
H-Index - 59
eISSN - 1439-0272
pISSN - 0303-4569
DOI - 10.1111/and.14031
Subject(s) - downregulation and upregulation , transcriptome , diabetes mellitus , erectile dysfunction , biology , gene , microbiology and biotechnology , medicine , endocrinology , gene expression , biochemistry
Diabetes mellitus erectile dysfunction (DMED) is a frequent complication of diabetes. Mesenchymal stem cell (MSC) therapy was demonstrated to improve erectile function in DMED. However, the pathogenesis of DMED and the mechanism by which MSCs function are still unclear. We established a rat model of DMED and gave MSC therapy through intracavernous injection. After transcriptome sequencing of rats’ penile tissue, we identified a total of 1,097 overlapped differentially expressed genes (DEGs) of the normal control group, DMED group, and MSC‐treated group, containing 189 upregulated genes and 908 downregulated genes. The enriched functions of upregulated DEGs included extracellular matrix organisation (GO:0030198), extracellular structure organisation (GO:0043062), and wound healing (GO:0042060), PPAR signalling pathway (rno03320), arachidonic acid metabolism (rno00590) and retinol metabolism (rno00830). The enriched functions of downregulated DEGs included peptidase activity (GO:0052547), hair follicle development (GO:0001942), intermediate filament‐based process (GO:0045103), nitrogen metabolism (rno00910), aldosterone‐regulated sodium reabsorption (rno04960) and retinol metabolism (rno00830). We constructed a PPI network with 547 nodes and 2,365 edges and identified 15 hub genes with high connectivity degree. In summary, 15 hub genes with potential roles in the development of ED were identified. Further functional research would be required to elucidate the molecular mechanism underlying misregulated genes.