X-J Liu1, X-G Bai, Y-L Teng, L Song, N Lu, R-Q Yang. 1. Department of Pathology, the First Hospital of Jilin University, Changchun City, Jilin Province, China. rui_qi_yang@sina.com.
Abstract
OBJECTIVE: miRNAs have been recently reported to contribute to the etiology of endometriosis in stem cells. However, the mechanisms remain unclear. The aim of this investigation is to explore the expression of miR-15a-5p and VEGFA in endometrial samples from patients with or without endometriosis. And then examine the regulation by miR-15a-5p on the expression of VEGFA. PATIENTS AND METHODS: Here we collected 31 endometrial samples from patients with or without endometriosis and characterized the miRNAs expression profiles of these two groups. Then, we investigated the regulation by microRNA-15a-5p (miR-15a-5p) on the expression of vascular endothelial growth factor (VEGF) in endometrial mesenchymal stem cells. RESULTS: It was demonstrated that there was dramatically down-regulation of miR-15a-5p in the patients with endometriosis, compared with control patients. Moreover, we found that the up-regulation of miR-15a-5p suppressed cell proliferation, migration and invasion of these ectopic stem cells by targeting the 3' untranslated region of VEGFA. CONCLUSIONS: Taken together, this newly identified miR-15a-5p module provides a new avenue to the understanding of the processes of endometriosis development, especially proliferation, motility as well as angiogenesis, and may facilitate the development of potential therapeutics against endometriosis.
OBJECTIVE: miRNAs have been recently reported to contribute to the etiology of endometriosis in stem cells. However, the mechanisms remain unclear. The aim of this investigation is to explore the expression of miR-15a-5p and VEGFA in endometrial samples from patients with or without endometriosis. And then examine the regulation by miR-15a-5p on the expression of VEGFA. PATIENTS AND METHODS: Here we collected 31 endometrial samples from patients with or without endometriosis and characterized the miRNAs expression profiles of these two groups. Then, we investigated the regulation by microRNA-15a-5p (miR-15a-5p) on the expression of vascular endothelial growth factor (VEGF) in endometrial mesenchymal stem cells. RESULTS: It was demonstrated that there was dramatically down-regulation of miR-15a-5p in the patients with endometriosis, compared with control patients. Moreover, we found that the up-regulation of miR-15a-5p suppressed cell proliferation, migration and invasion of these ectopic stem cells by targeting the 3' untranslated region of VEGFA. CONCLUSIONS: Taken together, this newly identified miR-15a-5p module provides a new avenue to the understanding of the processes of endometriosis development, especially proliferation, motility as well as angiogenesis, and may facilitate the development of potential therapeutics against endometriosis.