Silence of lncRNA MIAT protects ATDC5 cells against lipopolysaccharides challenge via up-regulating miR-132. Issue 1 (4th December 2019)

• Record Type: Journal Article
• Authors: Li, Chen; Pan, Su; Song, Yan; Li, Yinqing; Qu, Ji
• Is Part Of: Artificial cells, nanomedicine, and biotechnology. Volume 47:Issue 1(2019)
• Page Start: 2521
• Page End: 2527
• Publication Date: 2019-12-04
• Subjects: Inflammatory injury -- cytokines -- apoptosis -- NF-κB pathway -- JNK pathway; Artificial cells -- Periodicals; Nanotechnology -- Periodicals; Blood substitutes -- Periodicals; Tissue engineering -- Periodicals; Molecules -- Periodicals; Biotechnology -- Periodicals; 615.39
• DOI: 10.1080/21691401.2019.1626410
• Languages: English
• ISSNs: 2169-1401

Abstract

Abstract: 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-κB 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-κB and JNK pathways.