子宫内膜异位症
血管生成
小RNA
癌症研究
间充质干细胞
干细胞
发病机制
血管内皮生长因子A
异位表达
运动性
生物
医学
细胞生物学
血管内皮生长因子
内科学
免疫学
细胞培养
血管内皮生长因子受体
基因
遗传学
作者
Chia‐Yi Hsu,Tsung‐Hua Hsieh,Cheng‐Fang Tsai,Hung‐Pei Tsai,Hung‐Sheng Chen,Yu Chang,Hui‐Yu Chuang,Jau-Nan Lee,Ya‐Ling Hsu,Eing‐Mei Tsai
摘要
It is believed that endometrial miRNAs contribute to the aetiology of endometriosis in stem cells; however, the mechanisms remain unclear. Here we collected serum samples from patients with or without endometriosis and characterized the miRNA expression profiles of these two groups. MicroRNA-199a-5p (miR-199a-5p) was dramatically down-regulated in patients with endometriosis compared with control patients. In addition, we found that the tumour suppressor gene, SMAD4, could elevate miR-199a-5p expression in ectopic endometrial mesenchymal stem cells. Up-regulation of miR-199a-5p suppressed cell proliferation, motility and angiogenesis of these ectopic stem cells by targeting the 3' untranslated region of VEGFA. Furthermore, we established an animal model of endometriosis and found that miR-199a-5p could decrease the size of endometriotic lesions in vivo. Taken together, this newly identified miR-199a-5p module provides a new avenue to the understanding of the processes of endometriosis development, especially proliferation, motility and angiogenesis, and may facilitate the development of potential therapeutics against endometriosis.
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