However, the exact mechanism of endometriosis is unknown. Studies have shown that immunological changes play a significant role in the pathogenesis of endometriosis, leading to incomplete elimination of endometrial cells and the increased ability of endometrial lesions to be created and implant in the peritoneal cavity. However, retrograde menstruation occurs physiologically in almost 90% of healthy women, but less than one-fourth of them develop endometriosis. Nevertheless, the most accepted theory for the etiology of endometriosis is Sampson's theory, which suggests endometriosis develops as a result of retrograde menstruation through the fallopian tubes. Many genes possibly implicated in different physiopathological molecular mechanisms of endometriosis like steroidogenesis, inflammation and immune response, tissue remodeling and neoangiogenesis, metabolism regulation and DNA reparation. Besides, based on a recent study, the loss of the integrity of the gastrointestinal barrier might contribute to the pathogenesis of endometriosis through an increase in lipopolysaccharides (LPS) concentration. Recent studies have proven that endometriosis has a multifactorial etiology, with possible (epi)genetic, hormonal, and immunological factors as causes. The prevalence of endometriosis appears to have a range between 10 and 15% in the general population. Endometriosis is a common benign inflammatory disease that causes various symptoms such as chronic pelvic pain, dysmenorrhea, dyspareunia, and infertility. The presence of endometrial glands and stroma outside its normal site, the uterine cavity, is defined as endometriosis. The higher concentrations of mentioned cytokines in serum and PF and their higher expression by PFMCs and EESCs in endometriosis patients may contribute to the development of endometriosis. The gene and protein expression of HGF in PFMCs and its gene expression by EESCs were significantly higher in endometriotic women compared to controls ( P < 0.05– P < 0.01). The protein expression of MCP-1 and IGF-1 by PFMCs was statistically higher in endometriotic women ( P < 0.05 and P < 0.01, respectively). Gene expression of MCP-1 and IGF-1 in the PFMCs, PBMCs and EESCs also showed an increased level compared to controls ( P < 0.05 –P < 0.01). The levels of MCP-1, HGF, and IGF-1 in serum and PF in women with endometriosis were significantly higher than the controls ( P < 0.05– P < 0.001). The concentrations of mentioned cytokines in serum and PF, as well as their expression in PBMCs, PFMCs, EuESCs and EESCs from endometriosis patients and controls were assessed. To study the concentrations of monocyte chemoattractant protein-1 (MCP-1), hepatocyte growth factor (HGF), and insulin-like growth factor-1 (IGF-1) in peritoneal fluid (PF) and serum, and to evaluate their expressions by PF and peripheral blood mononuclear cells (PFMCs and PBMCs, respectively), and ectopic and eutopic endometrial stromal cells of patients with endometriosis (EESCs and EuESCs, respectively) compared with controls.
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