dysregulation of angiogenesis and inflammatory genes in endometrial mesenchymal stem cells and their contribution to endometriosis

Endometriosis is a common, chronic, inflammatory disorder in women, characterized by the presence of endometrial tissue outside the uterus cavity. the disease affects ~10% of women during their reproductive age. there are some debates on the pathogenesis of endometriosis and its mechanism among scientists; therefore, different hypotheses have been suggested. according to sampson's theory, a possible mechanism for seeding ectopic endometriotic lesions is a dysregulation of endometrial mesenchymal stem cells (emscs). in the present study, we evaluated the expression of candidate genes in emscs obtained from endometriosis patients and compared them with non-endometriosis female patients. in addition, bioinformatic analysis was conducted to uncover the genes in the list of our co-expression gene network in endometriosis. according to our results, the expression of vascular endothelial growth factor a, c-x-cmotif chemokine ligand 8, interleukin-6, and intercellular adhesion molecule-1 genes were upregulated in the emscs isolated from endometriosis patients. there was no significant difference in the expression of the laminb1 gene between the endometriosis and non-endometriosis patients. on the other hand, our bioinformatics analysis demonstrated that co-expressed genes were enriched in the cytokine signaling pathway. our study provides valuable insights into the gene expression dysregulation in emscs derived from endometriosis patients and suggests a possible function for co-expressed networks in the pathogenesis of endometriosis. to confirm the results, more investigations are required