A novel nude mouse model for studying the pathogenesis of endometriosis.

Endometriosis is a common female gynecological disease that is characterized by the presence of functional endometrial tissue outside the uterine cavity. At present, many animal models have been established. However, previous studies consistently use human endometrial tissue implanted in the subcutaneous or abdominal cavity for modeling and rarely use endometrial cells. In the present study, we ascertained whether immortalized stromal and/or epithelial endometrial cells are able to induce subcutaneous endometriosis in nude mice. Mixed human immortalized endometriosis stromal and epithelial cells, but not the cells of Group 1 or Group 2, were successfully constructed and led to endometriotic-like lesions. The endometriosis-like lesions observed in nude mice consisted of endometriosis-like glands lined with columnar epithelial cells and surrounded by stromal cells in the fibrous fatty connective tissue. Immunofluorescence analysis showed that glandular epithelial cells were intensely stained for E-cadherin and cytokeratin 7, and surrounding stromal cells were mildly stained for neprilysin (CD10) and vimentin. Moreover, the cells present in the endometriosis-like lesions were of human origin. Our data indicate that the mixture of human immortalized endometriosis stromal cells and epithelial cells is able to establish subcutaneous endometriosis lesions in nude mice. This model could be used to understand the molecular mechanisms involved in the occurrence and development of endometriosis.

Suppression of PRDX4 inhibits cell proliferation and invasion of ectopic endometrial stromal cells in endometriosis.

Oxidative stress (OS) has been proposed to play a role in the development of EMs. Peroxiredoxins are a family of antioxidant proteins that exhibit peroxidase activity in a thioredoxin-dependent manner, protecting cells against OS. The Western blotting results showed that the relative expression of PRDX4 was significantly increased in ectopic endometria compared with the normal endometria of EMs-free (p < .05). The H2O2 concentration was also significantly higher in the ectopic endometrium. PRDX4 siRNA was transfected into primary ectopic endometrial stromal cells (EESCs). The viability of the transfected EESCs was measured by CCK-8 assay, and the results showed significantly decreased cell viability. Furthermore, the apoptosis rate and ROS generation in flow cytometry assays were significantly increased after the knockdown of PRDX4 expression (p < .05). Scratch assays and transwell assays revealed that decreased expression of PRDX4 mediated by siRNA inhibited EESC migration and invasion. In conclusion, these findings indicate the potential role of PRDX4 in the development of EMs and PRDX4 as a possible therapeutic target for EMs treatment.