天狼星红
油红O
M2巨噬细胞
巨噬细胞极化
免疫染色
免疫印迹
巨噬细胞
贾纳斯激酶
小RNA
炎症
分子生物学
促炎细胞因子
吡喃结构域
医学
免疫学
细胞因子
生物
内分泌学
免疫组织化学
生物化学
体外
基因
炎症体
脂肪组织
脂肪生成
作者
Xiaowei Bian,Haoyang Peng,Wei Yin,Haizhou Guo,Gaofeng Shi
标识
DOI:10.1177/03000605231197071
摘要
Objective MicroRNA (miR)-22-3p is expressed in atherosclerosis (AS), but its function and regulatory mechanisms remain unclear. Therefore, the effects of miR-22-3p in AS were assessed in this study. Methods MiR-22-3p expression was assessed in AS, and miR-22-3p target genes were predicted using sequencing transcriptomics. The effect of miR-22-3p agomir on atherosclerotic lesions in an AS mouse model were determined by Oil red O, Masson’s, and sirius red staining, and by anti-smooth muscle actin and macrophage antigen-3 immunostaining. Gene expression in AS was evaluated by western blot and immunofluorescence. Results MiR-22-3p was expressed in AS and control samples (32.5% and 33.9% levels, respectively, relative to total miRNA among six highly expressed miRNAs). In the mouse model of AS, miR-22-3p agomir significantly reduced lipid deposition, proliferation of aortic collagen fibres, and macrophage content. Additionally, inducible nitric oxide synthase, interleukin-6, and tumour necrosis factor-α levels were significantly reduced, and levels of arginase 1 and CD206 were significantly enhanced. MiR-22-3p was found to target janus kinase 1( JAK1), and significantly inhibited the activation of NLR family pyrin domain containing 3 (NLRP3) and JAK1 in mice. Conclusions MiR-22-3p appears to reduce the inflammatory response in AS, which might be achieved by inducing the M2 macrophage phenotype and suppressing NLRP3 activation via JAK1.
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