MicroRNA-181c Inhibits Interleukin-6-mediated Beta Cell Apoptosis by Targeting TNF-α Expression

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ID: 111501
2019
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Abstract
We have previously reported that long-term treatment of beta cells with interleukin-6 (IL-6) is pro-apoptotic. However, little is known about the regulatory mechanisms that are involved. Therefore, we investigated pro-apoptotic changes in mRNA expression in beta cells in response to IL-6 treatment. We analyzed a microarray with RNA from INS-1 beta cells treated with IL-6, and found that TNF-α mRNA was significantly upregulated. Inhibition of TNF-α expression by neutralizing antibodies significantly decreased annexin V staining in cells compared with those treated with a control antibody. We identified three microRNAs that were differentially expressed in INS-1 cells incubated with IL-6. In particular, miR-181c was significantly downregulated in IL-6-treated cells compared with control cells and the decrease of miR-181c was attenuated by STAT-3 signaling inhibition. TNF-α mRNA was a direct target of miR-181c and upregulation of miR-181c by mimics, inhibited IL-6-induced increase in TNF-α mRNA expression. Consequently, reduction of TNF-α mRNA caused by miR-181c mimics enhanced cell viability in IL-6 treated INS-1 cells. These results demonstrated that miR-181c regulation of TNF-α expression plays a role in IL-6-induced beta cell apoptosis.
Reference Key
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Authors Yoon Sin Oh;Gong Deuk Bae;Eun-Young Park;Hee-Sook Jun;Oh, Yoon Sin;Bae, Gong Deuk;Park, Eun-Young;Jun, Hee-Sook;
Journal molecules
Year 2019
DOI
10.3390/molecules24071410
URL
https://doi.org/10.3390/molecules24071410
Keywords
interleukin-6 beta cell apoptosis microrna-181c Tumor National Center for Biotechnology Information NCBI NLM MEDLINE Mice animals pubmed abstract nih national institutes of health national library of medicine yoon sin oh hee-sook jun Rats cell line Gene Expression Regulation* micrornas / metabolism* apoptosis insulin-secreting cells / metabolism* pmid:30974824 pmc6480349 doi:10.3390/molecules24071410 gong deuk bae insulin-secreting cells / cytology interleukin-6 / metabolism* tumor necrosis factor-alpha / biosynthesis*

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