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RA滑膜成纤维样细胞外泌体促进巨噬细胞向M1极化

虞珊珊 李静 徐臻 成宇 宗明 范列英

同济大学学报(医学版)2023,Vol.44Issue(6):785-791,7.
同济大学学报(医学版)2023,Vol.44Issue(6):785-791,7.DOI:10.12289/j.issn.1008-0392.23239

RA滑膜成纤维样细胞外泌体促进巨噬细胞向M1极化

M1 polarization is induced by exosomes derived from fibroblast-like synoviocytes from patients with rheumatoid arthritis

虞珊珊 1李静 1徐臻 1成宇 1宗明 1范列英1

作者信息

  • 1. 同济大学附属东方医院检验科,上海 200120
  • 折叠

摘要

Abstract

Objective To investigate the role of exosomes derived from fibroblast-like synoviocytes from patients with rheumatoid arthritis(RA-FLS)in macrophage(Mø)polarization.Methods Synovial fluid and tissue from osteoarthritis(OA)patients(n=6)and rheumatoid arthritis(RA)patients(n=6)were collected,and the cytokines in joint fluid were detected using flow cytometry bead array(CBA)method.The expression of extracellular marker CD9 in the synovium was detected with immunohi-stochemical method.Primary synovial RA-FLS and OA-FLS were isolated,and the exosomes from cell-culture supernatant were identified by Western blotting and nanoparticle tracking analysis(NTA).The effects of OA-FLS and RA-FLS exosomes on the M1 and M2 phenotype genes were determined with real time fluorescence quantitative PCR(qRT-PCR)and CBA.Results The expressions of M1 type markers(IL-1 β,IL-6,IL-8),and M2 type marker(IL-10)in RA joint fluid were significantly higher than those in the OA group.High expression of CD9 was detected in RA synovium.RA-FLS was found to secrete more exosomes than OA-FLS.Elevated gene and protein expression levels of M1 markers were found in Mø treated with RA-FLS derived exosomes.Conclusion RA-FLS derived exosomes can induce M1 polarization in vitro.

关键词

类风湿关节炎/滑膜成纤维细胞/巨噬细胞/外泌体/M1型极化

Key words

rheumatoid arthritis/fibroblast-like synoviocytes/macrophage/exosome/M1 polarization

分类

医药卫生

引用本文复制引用

虞珊珊,李静,徐臻,成宇,宗明,范列英..RA滑膜成纤维样细胞外泌体促进巨噬细胞向M1极化[J].同济大学学报(医学版),2023,44(6):785-791,7.

基金项目

国家自然科学基金面上项目(81971535) (81971535)

上海市浦东新区卫生系统优秀青年医学人才培养计划(PWRq2020-21) (PWRq2020-21)

上海市"医苑新星"青年医学人才培养资助计划(YYXX202101) (YYXX202101)

同济大学学报(医学版)

OACSTPCD

1008-0392

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