Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132

被引:18
作者
Li, Chen [1 ]
Pan, Su [1 ]
Song, Yan [2 ]
Li, Yinqing [2 ]
Qu, Ji [1 ]
机构
[1] Jilin Univ, Orthopaed Med Ctr, Hosp 2, 218 Zigiang St, Changchun 130041, Jilin, Peoples R China
[2] Changchun Univ Chinese Med, Changchun, Jilin, Peoples R China
关键词
Inflammatory injury; cytokines; apoptosis; NE-kappa B pathway; JNK pathway; NONCODING RNA MIAT; COMPETITIVELY BINDING; SIGNALING PATHWAY; EXPRESSION; ATHEROSCLEROSIS; INJURY;
D O I
10.1080/21691401.2019.1626410
中图分类号
Q81 [生物工程学(生物技术)]; Q93 [微生物学];
学科分类号
071005 ; 0836 ; 090102 ; 100705 ;
摘要
The over-expanding role of lncRNA myocardial infarction associated transcript (MIAT) in various human diseases has been recently revealed. This study attempted to see the role of MIAT in a cell model of osteoarthritis (OA). ATDC5 cells were subjected to lipopolysaccharides (LPS) to mimic a cell model of OA. The effects of MIAT on the model were tested by performing CCK-8 assay, flow cytometry, qRT-PCR, western blot and ELISA. The downstream miRNA and signalling pathways were studied by utilizing qRT-PCR and western blot. Transfection of ATDC5 cells with the shRNA specific against MIAT significantly attenuated LPS-evoked apoptosis and cytokines release. At the meantime, the viability loss and the cleavage of caspases were ameliorated as well. MIAT overexpressed lead to the opposite result. Further, miR-132 was found to be negatively regulated by MIAT. The protective effects of MIAT silence were flattened when miR-132 expression was suppressed. Besides that the inhibitory effects of MIAT silence on LPS-evoked NF-kappa B and JNK activation were eliminated by miR-132 silence. This study illustrated that silence of MIAT protected ATDC5 cells against LPS challenge. The chondroprotective effects of MIAT silence may be via up-regulation of miR-132 and inhibition of NF-kappa B and JNK pathways.
引用
收藏
页码:2521 / 2527
页数:7
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