细胞凋亡
细胞生长
基因敲除
小RNA
成纤维细胞
细胞周期
异位表达
化学
类风湿性关节炎
细胞
癌症研究
滑膜
免疫印迹
细胞生物学
分子生物学
免疫学
生物
基因
生物化学
体外
作者
Yi-Xuan Liu,XL Zhang,Xian‐Fang Li,Y-C Tang,Xiwa Zhao
出处
期刊:PubMed
日期:2018-01-01
卷期号:22 (2): 461-471
被引量:30
标识
DOI:10.26355/eurrev_201801_14196
摘要
Several microRNAs have been reported to contribute the progression of rheumatoid arthritis (RA) due to the ectopic expression of miRNAs in fibroblast-like synoviocytes (FLS). However, the function of miR-212-3p in RA still has not been mentioned before.We obtained serum, synovial tissues, and FLS samples from RA patients and normal donors. Quantitative Real-time polymerase chain reaction (qRT-PCR) was used to analysis the expression level of miR-212-3p. By using miR-212-3p mimics and inhibitors, we detected the effects of miR-212-3p on cell proliferation, cell cycle, and apoptosis in RA-FLS. Dual-luciferase and Western-blot were employed to verify the target of miR-212-3p. In addition, we over-expressed the SOX5 in miR-212-3p mimics treatment FLS to emphasize our results.The level of miR-212-3p in serum, synovial tissues, and FLS from RA patients was lower than these in relative normal group. Up-regulation of miR-212-3p inhibited cell proliferation, promoted cell apoptosis; however, knockdown of miR-212-3p promoted cell growth but reduced cell apoptotic rate. Furthermore, we found SOX5 as a direct target of miR-212-3p in RA-FLS and up-regulation of SOX5 reversed the effects of miR-212-3p over-expression.miR-212-3p could reduce cell proliferation and promoted cell apoptosis of RA-FLS via repressing SOX5, which may provide a new biological target for RA treatment.
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