Endometriosis is a common disorder of unknown etiology, and non-surgical therapies are still a challenge. To understand the pathogenesis and preclinical testing of drugs for endometriosis, animal models are highly desirous. Herein, we carried out longitudinal characterization of a mouse model for endometriosis where uterine tissue was transplanted onto the intestinal mesentery. During the course of lesion development from day 15 to 60 post-induction, the ectopic endometrium became pale, fluid-filled and the animals developed peritoneal adhesions. Most lesions resembled a well-differentiated type of endometriosis and ~ 13% of animals had mixed type of lesions. There was extensive stromal compaction in the ectopic tissue. During the progression of endometriosis, there was increased proliferation of epithelial and stromal cells as evident by PCNA staining. Cyp19a1 (aromatase) mRNA was detected in the ectopic lesions on day 15 and 30 post-induction of endometriosis, by day 60 the expression was reduced. As compared to the control endometrium, the mRNA levels of Esr1 progressively reduced while the levels of inflammation associated genes ( Esr2, Ifng, Tnf and Il1b) increased in the ectopic lesions. Infiltration of macrophages and polymorphonuclear leucocytes was also observed in the ectopic lesions indicative of inflammation. As compared to control, there was no change in levels of Cytokeratin and E-cadherin in the epithelial cells of ectopic endometrium. We did not observe excessive collagen deposition or α-SMA positive myofibroblasts in the stroma of the ectopic endometrium. Thus, epithelial-to-mesenchymal transition and fibrosis are not detected in the mouse model of endometriosis. Our results show that the mouse model of endometriosis mimics some but not all the features of human endometriosis.

中文翻译：

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子宫内膜异位症小鼠模型的特征是增殖和炎症，但不是上皮间质转化和纤维化

子宫内膜异位症是一种病因不明的常见疾病，非手术治疗仍然是一个挑战。为了了解子宫内膜异位症药物的发病机制和临床前试验，非常需要动物模型。在此，我们对子宫组织移植到肠系膜上的子宫内膜异位症小鼠模型进行了纵向表征。在诱导后第 15 天至第 60 天的病变发展过程中，异位子宫内膜变得苍白、充满液体并且动物发生腹膜粘连。大多数病变类似于分化良好的子宫内膜异位症，约 13% 的动物具有混合型病变。异位组织中存在广泛的基质压实。在子宫内膜异位症的发展过程中，PCNA染色表明上皮细胞和基质细胞增殖增加。在子宫内膜异位症诱导后第 15 天和第 30 天的异位病变中检测到 Cyp19a1（芳香化酶）mRNA，到第 60 天表达降低。与对照子宫内膜相比，Esr1 的 mRNA 水平逐渐降低，而异位病变中炎症相关基因（Esr2、Ifng、Tnf 和 Il1b）的水平增加。在指示炎症的异位病变中也观察到巨噬细胞和多形核白细胞的浸润。与对照相比，异位子宫内膜上皮细胞中细胞角蛋白和E-钙粘蛋白的水平没有变化。我们没有在异位子宫内膜的基质中观察到过多的胶原沉积或 α-SMA 阳性肌成纤维细胞。因此，在子宫内膜异位症小鼠模型中未检测到上皮间质转化和纤维化。我们的结果表明，子宫内膜异位症的小鼠模型模仿了人类子宫内膜异位症的一些但不是全部特征。