IL-6-miR-210 Suppresses Regulatory T Cell Function and Promotes Atrial Fibrosis by Targeting Foxp3

• Published in: Molecules and cells 2020, 43(5), , pp.438-447
• Main Authors: Chen, YingWei, Chang, GuoDong, Chen, XiaoJie, Li, YunPeng, Li, HaiYu, Cheng, Dong, Tang, Yi, Sang, HaiQiang
• Format: Article
• Language: English
• Subjects: Atrial Fibrillation - genetics; Atrial Fibrillation - immunology; Cells, Cultured; Fibrosis; Forkhead Transcription Factors - genetics; Forkhead Transcription Factors - metabolism; Gene Expression Regulation; Heart Atria - pathology; Humans; Immune Tolerance; Interleukin-2 Receptor alpha Subunit - metabolism; Interleukin-6 - genetics; Interleukin-6 - metabolism; MicroRNAs - genetics; T-Lymphocytes, Regulatory - immunology; 생물학
• ISSN: 1016-8478; 0219-1032
• DOI: 10.14348/molcells.2019.2275

The aim of this study was to explore the role of IL-6-miR-210 in the regulation of Tregs function and atrial fibrosis in atrial fibrillation (AF). The levels of interleukin (IL)-6 and IL-10 in AF patients were detected by using ELISA. Proportions of Treg cells were detected by fluorescence activated cell sorting analysis in AF patients. The expression of Foxp3, α-SMA, collagen I and collagen III were determined by western blot. The atrial mechanocytes were authenticated by vimentin immunostaining. The expression of miR-210 was performed by quantitative real-time polymerase chain reaction (qRT-PCR). TargetScan was used to predict potential targets of miR-210. The cardiomyocyte transverse sections in AF model group were observed by H&E staining. The myocardial filaments were observed by masson staining. The level of IL-6 was highly increased while the level of IL-10 (Tregs) was significantly decreased in AF patients as compared to normal control subjects, and IL-6 suppressed Tregs function and promoted the expression of α-SMA, collagen I and collagen III. Furthermore, miR-210 regulated Tregs function by targeting Foxp3, and IL-6 promoted expression of miR-210 via regulating hypoxia inducible factor-1α (HIF-1α). IL-6-miR-210 suppresses regulatory T cell function and promotes atrial fibrosis by targeting Foxp3.