Mechanism of endometrial cell survival in the formation of endometriotic lesion

子宫内膜异位症是一种顽固性疾病，其特征是子宫腔外存在子宫内膜组织。在我们的实验性内出血小鼠模型中，明显的子宫内膜异位症样病变表现出高水平的炎症因子表达。为了确定子宫内膜异位症样病变中蛋白质水平的变化，将蛋白质谱变化与对照组（无出血）小鼠进行比较。通过二维凝胶电泳和MALDI-TOF质谱分析uOVX和对照小鼠病变细胞裂解液，结果显示，在uOVX小鼠病变中α - 1抗胰蛋白酶（a1-AT）水平降低。在培养的基质细胞中，a1-AT抑制炎症和细胞存活因子的表达。a1-AT水平降低可加重局部炎症，提示a1-AT可能参与子宫内膜异位症的病理生理。

Endometriosis is the intractable disorder characterized by the presence of endometrial tissue outside of the uterine cavity. Distinct endometriosis-like lesions in our experimental internal bleeding mouse model exhibited the expression of high levels of inflammation factors. To identify changes in protein levels in endometriosis-like lesions, protein profile changes were compared with control (no bleeding) mice. Cell lysates from lesions from uOVX and control mice were analyzed by 2-D gel electrophoresis, followed by MALDI-TOF MS. The level of alpha1-antitrypsin (a1-AT) is decreased in lesions from mice that underwent uOVX. In cultured stromal cells, a1-AT inhibited the expression of inflammation and cell survival factors. Reduced a1-AT levels may exacerbate local inflammation, suggesting the possible involvement of a1-AT in the pathophysiology of endometriosis.