Hypothesis / aims of study
Pelvic organ prolapse (POP) refers to a group of diseases in which the pelvic organs and the adjacent vaginal wall decrease due to weakened pelvic support tissue. Although it rarely causes severe symptoms or death, it has a huge impact on the quality of life of patients. Based on the diversity and heterogeneity of the pathophysiology of POP, its molecular mechanism remains unclear. In order to identify candidate genes in the occurrence and progression of POP, we have mined and analyzed some differential genes from public databases.
Study design, materials and methods
microarray datasets GSE53868, from Prolapsed and non-prolapsed position in the vaginal wall of 12 POP patients, was downloaded from Gene Expression Omnibus (GEO) database. The differentially expressed genes (DEGs) were selected and identified, and Kyoto Encyclopedia of Genes and Genomes (KEGG) and Gene ontology (GO) function enrichment analyses were performed by the Database for Annotation, Visualization and Integrated Discovery (DAVID). The protein-protein interaction network (PPI) was constructed using STRING online website and the module analysis was performed with Cytoscape software, while hub genes were identified by MCODE plugin in Cytoscape.
Interpretation of results
Thrombomodulin is a specific endothelial cell receptor responsible for the conversion of protein C to the activated protein C (protein Ca). Once evolved, protein Ca scissions the activated cofactors of the coagulation mechanism, factor Va and factor VIIIa, and thereby reduces the amount of thrombin generated. Unfortunately, we did not find a direct link between POP pathological process and coagulation function
Zinc finger protein SNAI1 Involved in induction of the epithelial to mesenchymal transition (EMT), formation and maintenance of embryonic mesoderm, growth arrest, survival and cell migration. SNAI1 participated in the activation of fibroblasts while POP is closely related to fibroblast and collagen metabolism disorders.