ADAM10型
下调和上调
癌症研究
荧光素酶
类风湿性关节炎
调节器
化学
成纤维细胞
活力测定
关节炎
小RNA
报告基因
转染
炎症
细胞生物学
细胞
基因表达
生物
免疫学
体外
金属蛋白酶
基因
生物化学
基质金属蛋白酶
去整合素
作者
Zikang Xie,Shen Peng-fei,Yuxing Qu,Jianda Xu,Chong Zheng,Yi Gao,Bin Wang
摘要
MiR-20a has been reported as a key regulator to pro-inflammatory factor release in fibroblast-like synoviocytes (FLS), which caused rheumatoid arthritis (RA). However, the molecular mechanism of miR-20a in RA remains to be further elucidated. This study aimed to investigate the roles of miR-20a in RA pathology. RA (n = 24) and osteoarthritis (OA, n = 20) and normal healthy tissues (n = 16) were collected from operation. TargetScan and dual-luciferase reporter were performed to predict and confirm the potential binding sites of miR-20a on ADAM metallopeptidase domain 10 (ADAM10). Pearson's analysis was adopted to evaluate the correlation between miR-20a and ADAM10 expression. It was found that MiR-20a was downregulated in RA tissues, and overexpressed miR-20a inhibited cell viability, migration and invasion, and the expression of inflammatory factors in RA-FLS MH7A cells. ADAM10 was identified as the target gene of miR-20a, and upregulation of ADAM10 reversed the inhibitory effects of miR-20a. In conclusion, miR-20a inhibits the progression of RA-FLS as well as the inflammatory factor expression by targeting ADAM10.
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