ABSTRACT
Epididymitis is a commonly diagnosed disease associated with male infertility. However, little is known about the molecules that are involved in its development. This study was to identify critical genes associated with lipopolysaccharide-induced epididymitis and analyze the molecular mechanism of epididymitis through RNA sequencing. Experimental epididymitis models were generated by administering male Sprague-Dawley rats' lipopolysaccharide. A total of 1378 differentially expressed genes, including 531 upregulated and 847 downregulated genes, were identified in the epididymitis model rats compared with those in sham-operated rats by RNA sequencing. Functional enrichment analyses suggested that the upregulated genes were markedly enriched in inflammation-related biological processes, as well as in the tumor necrosis factor (TNF) signaling pathway, cytokine-cytokine receptor interactions, complement and coagulation cascades, and in the chemokine signaling pathway. Four downregulated genes (collagen type XXVIII alpha 1 chain [Col28α1], cyclin-dependent kinase-like 1 [Cdkl1], phosphoserine phosphatase [Psph], and fatty acid desaturase 2 [Fads2]) and ten upregulated genes (CCAAT/enhancer-binding protein beta [Cebpβ], C-X-C motif chemokine receptor 2 [Cxcr2], interleukin 11 [Il11], C-C motif chemokine ligand 20 [Ccl20], nuclear factor-kappa-B inhibitor alpha [Nfkbiα], claudin 4 [Cldn4], matrix metallopeptidase 9 [Mmp9], heat shock 70 kDa protein 8 [Hspa8], intercellular cell adhesion molecule-1 [Icam1], and Jun) were successfully confirmed by real-time polymerase chain reaction. Western blot demonstrated that CDKL1 was decreased, while MMP9 and NFKBIA were increased in the experimental model group compared with those in the sham-operated group. Our study sheds new light on the understanding of the early response of the epididymis during bacterial epididymitis.
Subject(s)
Animals , Male , Rats , Base Sequence/genetics , Disease Models, Animal , Enzyme-Linked Immunosorbent Assay , Epididymis/metabolism , Epididymitis/metabolism , Gene Expression Profiling , Genes/genetics , Lipopolysaccharides/pharmacology , Rats, Sprague-Dawley , Real-Time Polymerase Chain Reaction , Sequence Analysis, RNAABSTRACT
Spermatogenesis originates from spermatogonial stem cells (SSCs). SSCs can continually renew and eventually differentiate into spermatozoa under control of various growth factors, microenvironments and self-signaling. The molecules involved in SSCs self-renewal include glial cell-derived nerve growth factor, fibroblast growth factor and downstream signaling pathways, as well as the transcription factors and the epigenetic regulators. Molecules related to SSCs differentiation include retinoic acid, a variety of transcription factors and the eptigenetic regulatory factors. The research on the mechanism of SSCs self-renewal and differentiation is of great significance for the understanding of spermatogenesis and the diagnosis and treatment of male infertility. This review summarized the exogenous factors, transcription factors, and epigenetic regulators that are involved in the regulation of SSCs self-renewal and differentiation in recent years.
ABSTRACT
Spermatogenesis originates from spermatogonial stem cells (SSCs).SSCs can continually renew and eventually differentiate into spermatozoa under control of various growth factors,microenvironments and self-signaling.The molecules involved in SSCs self-renewal include glial cell-derived nerve growth factor,fibroblast growth factor and downstream signaling pathways,as well as the transcription factors and the epigenetic regulators.Molecules related to SSCs differentiation include retinoic acid,a variety of transcription factors and the eptigenetic regulatory factors.The research on the mechanism of SSCs self-renewal and differentiation is of great significance for the understanding of spermatogenesis and the diagnosis and treatment of male infertility.This review summarized the exogenous factors,transcription factors,and epigenetic regulators that are involved in the regulation of SSCs self-renewal and differentiation in recent years.