BACKGROUND 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. 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). METHODS Stromal 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. RESULTS Significantly 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). CONCLUSIONS These findings suggest reduced propensity to apoptosis and increased angiogenesis potential of EESCs, which may be involved in pathogenesis of endometriosis.

中文翻译：

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与非子宫内膜异位对照相比，子宫内膜异位患者异位和异位基质细胞凋亡和血管生成的评估。

背景技术子宫内膜异位症是一种以子宫内膜组织子宫外生长为特征的慢性，疼痛和炎性疾病。血管生成的增加和对细胞凋亡的抗性已被认为与子宫内膜异位症的发病机制和发展有关。这项研究的目的是检查子宫内膜异位症患者的子宫内膜基质细胞与非子宫内膜异位对照（CESCs）的子宫内膜基质细胞的凋亡潜力以及异位（EuESCs）和异位（EESCs）子宫内膜基质细胞的凋亡潜力和血管生成的贡献。方法通过酶消化法从经腹腔镜确认的子宫内膜异位患者的异位（n = 11）和异位（n = 17）子宫内膜组织中分离基质细胞。15例非子宫内膜异位症患者的子宫内膜基质细胞作为对照。通过免疫荧光染色和使用一组抗体的流式细胞仪对细胞进行表征后，从培养的细胞中分离出总RNA，并分析涉及凋亡的基因（Bcl-2，Bcl-xL，Bax和caspase-3）的表达实时荧光定量PCR）和血管生成[血管内皮生长因子-A（VEGF-A）和肝细胞生长因子（HGF）]。结果在EESC中发现的Bcl-2和Bcl-xL基因表达水平明显高于EuESC和CESC（p <0.01）。Bax在EESC，EuESC和CESC中的基因表达没有统计学意义。此外，与CESCs（p <0.01）或EESCs（p <0.05）相比，EuESCs的caspase-3基因表达明显降低。关于血管生成，VEGF-A基因在EESCs（p <0.001）和EuESCs（p <0.）中的表达。05）明显高于CESC。与EuESCs相比，EESCs的HGF基因表达明显更高（p <0.05）。结论这些发现表明，ESCS的凋亡倾向降低，血管生成潜力增加，这可能与子宫内膜异位症的发病机理有关。