MicroRNA-181c Inhibits Interleukin-6-mediated Beta Cell Apoptosis by Targeting TNF-alpha Expression
- Authors
- Oh, Yoon Sin; Bae, Gong Deuk; Park, Eun-Young; Jun, Hee-Sook
- Issue Date
- 10-Apr-2019
- Publisher
- MDPI
- Keywords
- Interleukin-6; beta cell apoptosis; microRNA-181c
- Citation
- MOLECULES, v.24, no.7
- Journal Title
- MOLECULES
- Volume
- 24
- Number
- 7
- URI
- https://scholarworks.bwise.kr/gachon/handle/2020.sw.gachon/1587
- DOI
- 10.3390/molecules24071410
- ISSN
- 1420-3049
- 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-alpha mRNA was significantly upregulated. Inhibition of TNF-alpha 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-alpha mRNA was a direct target of miR-181c and upregulation of miR-181c by mimics, inhibited IL-6-induced increase in TNF-alpha mRNA expression. Consequently, reduction of TNF-alpha 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-alpha expression plays a role in IL-6-induced beta cell apoptosis.
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