Abstract
BackgroundEndometriosis is a chronic, painful, and inflammatory disease characterized by extra-uterine growth of endometrial tissues. Increased angiogenesis and resistance to apoptosis have been suggested to be involved in pathogenesis and development of endometriosis. The objective of this study was to examine apoptosis potential and angiogenesis contribution of eutopic (EuESCs) and ectopic (EESCs) endometrial stromal cells in patients with endometriosis compared to endometrial stromal cells from non-endometriotic controls (CESCs).MethodsStromal cells were isolated by enzymatic digestion of ectopic (n = 11) and eutopic (n = 17) endometrial tissues from laparoscopically-confirmed endometriotic patients. Endometrial stromal cells of 15 non-endometriotic patients served as control. Following cell characterization by immunofluorescent staining and flow cytometry using a panel of antibodies, the total RNA was isolated from the cultured cells, and analyzed for the expression of genes involved in apoptosis (Bcl-2, Bcl-xL, Bax, and caspase-3) and angiogenesis [vascular endothelial growth factor-A (VEGF-A) and hepatocyte growth factor (HGF)] by Real-time PCR.ResultsSignificantly higher gene expression levels of Bcl-2 and Bcl-xL were found in EESCs compared with EuESCs and CESCs (p < 0.01). The gene expression of Bax in EESCs, EuESCs, and CESCs was not statistically significant. Furthermore, EuESCs exhibited a significantly lower caspase-3 gene expression compared with CESCs (p < 0.01) or EESCs (p < 0.05). Regarding angiogenesis, VEGF-A gene expression in EESCs (p < 0.001) and EuESCs (p < 0.05) were significantly higher compared with those of CESCs. EESCs exhibited a significantly higher HGF gene expression compared with EuESCs (p < 0.05).ConclusionsThese findings suggest reduced propensity to apoptosis and increased angiogenesis potential of EESCs, which may be involved in pathogenesis of endometriosis.
Highlights
Endometriosis is a chronic, painful, and inflammatory disease characterized by extra-uterine growth of endometrial tissues
Our results showed significantly higher gene expression levels of B-cell lymphoma/ leukemia-2 (Bcl-2) (Fig. 2a) and B-cell lymphoma-extra Large (Bcl-xL) (Fig. 2b) in Ectopic Endometrial Stromal Cells (EESCs) compared to eutopic endometrial stromal cells (EuESCs) or cells from non-endometriotic controls (CESCs) (p < 0.01)
The results of our study showed significantly higher gene expression levels of anti-apoptotic proteins, Bcl-2 and Bcl-xL, in EESCs compared with EuESCs or CESCs
Summary
Endometriosis is a chronic, painful, and inflammatory disease characterized by extra-uterine growth of endometrial tissues. Increased angiogenesis and resistance to apoptosis have been suggested to be involved in pathogenesis and development of endometriosis. Endometriosis, defined as settlement of endometrial glands and stroma in the extra-uterine cavity, is associated with irregular uterine bleeding, infertility, dyspareunia, and chronic pelvic pain [1]. Several theories have been developed to address the pathogenesis of endometriosis, but the retrograde menstruation proposed by Sampson in 1927 is the most widely accepted one [4]. According to this theory, uterine endometrial cells refluxed through fallopian tubes into the peritoneal cavity during menstruation, implant and initiate the endometriotic lesion formation. Endometrial cells are likely to play an important role in the establishment of the disease [5]
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