ISSN: 2157-7013
+44 1300 500008
Chia-Yi Hsu and Eing-Mei Tsai
Posters: J Cell Sci Ther
Endometriosis, defi ned as the presence and growth of functional endometrial tissues outside the uterine cavity, is a common benign gynecological disease that aff ects 10-15% of reproductive aged women. Th e pathophysiology of endometriosis is not clearly understood. MicroRNAs (miRNAs) are small (19 to 25 nts) endogenous non-coding RNA molecules that post-transcriptionally regulate gene expression. In previously study, we found cox2 played a role in the pathogenesis in the endometriosis. We predicted microRNA-199a is the upregulator of cox2. Further study of the role of microRNA in the development of endometriosis is investigated by using eutopic and ectopic endometrial mesenchymal stem cells. First, we assessed the microRNA-199a expression level by real-time PCR in human serum of women with (n=58) and without (n=27) endometriosis. Th e data showed that the microRNA-199a expression was signifi cantly higher in endometriosis compare to those without endometriosis. Th e microRNA-199a expression in endometrial mesenchymal stem cells (MSCs) of eutopic and ectopic from the same endometrial donor was investigated. Further,we identify the biofunction of microRNA on cell migration, invasion and proliferation by wound healing assay, Matrigel invasion assay, and XTT assay, respectively, in endometrial MSCs. Silencing of microRNA-199a in ectopic endometrial MSCs led to decreased cell migration, invasion and proliferation. In addition to, introducing the microRNA-199a into the eutopic endometrial MSCs could increase cell motility and growth. Th ese data indicated that the microRNA-199a has signifi cant eff ect on endometriosis progression. Our study revealed the serum microRNA-199a levels were signifi cantly higher in the endometriosis cases. Th e expression levels of the microRNA-199a were related to cell motility and growth in eutopic and ectopic endometrial MSCs. Th ese results suggest the microRNA- 199a could play a role in the development of endometriosis