Mouse GRO-alpha, KC

Clear cell renal cell carcinoma (ccRCC) is the most common subtype among renal cancer, and more and more researches find that the occurrence of ccRCC is associated with genetic changes, but the molecular mechanism still remains unclear. The present study aimed to identify aggregation trend of differentially expressed genes (DEGs) in ccRCC, which would be beneficial to the treatment of ccRCC and provide research ideas using a series of bioinformatics approach. Gene ontology (GO) and Kyoto Encyclopedia of Gene and Genomes (KEGG) analysis were used to get the enrichment trend of DEGs of GSE53757 and GSE16449. Draw Venn Diagram was applied for co-expression of DEGs. Cytoscape with the Retrieval of Interacting Gene (STRING) datasets and Molecular Complex Detection (MCODE) were performed protein-protein interaction (PPI) of DEGs. The Kaplan-Meier Plotter analysis of top 15 upregulated and top 15 downregulated were selected in Gene Expression Profiling Interactive Analysis (GEPIA). Then, the expression level of hub genes between normal renal tissue and different pathological stages of ccRCC tissue, which significantly correlated with overall survival in ccRCC patients, were also analyzed by Ualcan based on The Cancer Genome Atlas (TCGA) database. In this study, we got 167 co-expression DEGs, including 72 upregulated DEGs and 95 downregulated DEGs. We identified 11 hub genes had significantly correlated with overall survival in ccRCC patients. Among them, KIF23, APLN, ADCY1, GREB1, TLR4, IRF8, CXCL1, CXCL2, deserved our attention.

Endometriosis is a chronic gynecological disorder, characterized by the presence of ectopic endometrial tissue outside the uterine cavity. Among several hypotheses, Sampson's theory of retrograde menstruation is still applicable. Recent studies have reported the importance of inflammation among endometrial tissue, the peritoneum, and immune cells. However, less is known regarding the role of bacterial infection in the pathophysiology of endometriosis. We hypothesized that Ureaplasma urealyticum infection might contribute to the development of endometriosis by inducing the production of inflammatory mediators by peritoneal mesothelial cells (PMCs), possibly through TLR2. Hence, our objective was to reveal whether PMC infection by U. urealyticum is associated with endometriosis. Moreover, we aimed to demonstrate the molecular mechanism involved in this relationship. We developed a new infection-induced mouse model of endometriosis with wild type and Tlr2-deficient mice. Based on the in vivo mouse model, U. urealyticum-infected mice showed significantly increased numbers and sizes of ectopic endometriotic lesions. U. urealyticum upregulated not only the production of IL-6, CXCL1, and CCL2, but also the expression of ICAM-1, VCAM-1, and MMP2 in murine PMCs. Similarly, endometrial stromal cells dose-dependently produced IL-6, CXCL1, and CCL2 in response to U. urealyticum infection. The series of inflammatory responses in PMCs was mediated mainly through TLR2. The phosphorylation of ERK and JNK was observed when U. urealyticum was added to PMCs and knock out of Tlr2 inhibited these MAPKs phosphorylation. Based on our co-culture study, U. urealyticum-infected PMCs exhibited significantly increased attachment to ESCs compared with uninfected PMCs. Collectively, U. urealyticum infection promotes the development of endometriosis by increasing inflammatory mediators, adhesion molecules, and MMP-2 expression in PMCs through TLR2 signaling. Through our results, we present a theory that infection-induced pelvic inflammation contributes to the initiation and progression of endometriosis. Appropriate treatment of reproductive tract infection may decrease the prevalence of endometriosis.