METTL17-Mediated Inhibition of M1 Macrophage Polarization Alleviates the Progression of Ankylosing Spondylitis.

IF 1.5 4区 医学 Q4 BIOTECHNOLOGY & APPLIED MICROBIOLOGY
Jiang-Tao Lv, Ying-Ying Zhang, Shao-Qi Tian, Jiang-Jun Liu
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引用次数: 0

Abstract

RNA methylation is involved in the pathogenesis of ankylosing spondylitis (AS). This study aimed to investigate the potentials of METTL17 in AS. mRNA expression was detected using RT-qPCR. RNA methylation was detected using MeRIP assay. Protein expression was detected using western blot. Cell proliferation was detected using EdU assay. Macrophage functions was detected using flow cytometry. METTL17 was upregulated after exposure to LPS. However, METTL17 knockdown promoted inflammatory response. Moreover, METTL17 knockdown promoted M1 macrophage polarization. Mechanically, METTL17 regulate RNA methylation. Mechanically, METTL17 promoted the RNA methylation of STAT1, inhibiting the mRNA and protein stability of STAT1. In summary, METTL17 inhibits inflammatory response and M1 macrophage polarization via mediating the RNA methylation of STAT1. Therefore, targeting METTL17/STAT1 may be a promising strategy for AS.

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来源期刊
Critical Reviews in Eukaryotic Gene Expression
Critical Reviews in Eukaryotic Gene Expression 生物-生物工程与应用微生物
CiteScore
2.70
自引率
0.00%
发文量
67
审稿时长
1 months
期刊介绍: Critical ReviewsTM in Eukaryotic Gene Expression presents timely concepts and experimental approaches that are contributing to rapid advances in our mechanistic understanding of gene regulation, organization, and structure within the contexts of biological control and the diagnosis/treatment of disease. The journal provides in-depth critical reviews, on well-defined topics of immediate interest, written by recognized specialists in the field. Extensive literature citations provide a comprehensive information resource. Reviews are developed from an historical perspective and suggest directions that can be anticipated. Strengths as well as limitations of methodologies and experimental strategies are considered.
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