JCC:M2巨噬细胞通过外泌体miR-590-3p减弱结肠粘膜损伤并促进上皮修复

2020-10-21 MedSci原创 MedSci原创

M1巨噬细胞是可以产生促炎细胞因子的巨噬细胞,被称为经典型巨噬细胞,具有很强的杀死微生物特性,但是这些特异也容易引起组织破坏。

        M1巨噬细胞是可以产生促炎细胞因子的巨噬细胞,被称为经典型巨噬细胞,具有很强的杀死微生物特性,但是这些特异也容易引起组织破坏。M2巨噬细胞,又称替代性活化巨噬细胞,在对寄生虫、组织重塑、血管生成和过敏性疾病的反应中起着核心作用,参与炎症的消退和肠道修复。而巨噬细胞分泌的外泌体正在成为粘膜微环境中细胞间通讯的重要介质。本项研究旨在探究巨噬细胞与外泌体分泌在修复肠道损伤中的作用。

 

        研究人员对M2巨噬细胞进行miR-590-3p的转染,分离并鉴定了来源于M2巨噬细胞的外泌体成分。在体外测试肠上皮细胞的增殖和伤口愈合情况,并在各组之间进行比较。通过使用质粒转染,western印迹,免疫荧光和荧光素酶报告基因检测研究了LATS1和β-catenin信号转导的机制在外泌体和组织修复之间的关系。

 

        研究人员最后证明了M2巨噬细胞以外泌体依赖性方式促进结肠上皮细胞增殖。上皮细胞介导M2巨噬细胞衍生的外泌体在上皮增殖中的作用。此外,富含巨噬细胞外泌体的miR-590-3p可以从巨噬细胞转移到上皮细胞中,从而增强上皮细胞的增殖和伤口愈合。从机制上讲,miR-590-3p通过与LATS1的编码序列结合来抑制LATS1的表达,并随后激活YAP /β-catenin调节的转录过程,以改善上皮细胞伤口愈合的能力。MiR-590-3p还抑制诱导炎症的细胞因子,包括TNF-α,IL-1β和IL-6的一系列促炎因子。

 

        研究最后作者说道:M2巨噬细胞衍生的外泌体miR-590-3p通过靶向刺激LATS1位点并随后激活YAP /β-catenin调控的转录来减少炎症信号并促进上皮再生,这可能为溃疡性结肠炎(UC)的治疗提供新的靶点。

 

 

原始出处 :

Feihong Deng. Et al. M2 macrophage-derived exosomal-miR-590-3p attenuates DSS-induced mucosal damage and promotes epithelial repair via the LATS1/YAP/β-catenin signalling axis. Journal of Crohn's and Colitis.2020.

 

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    2021-03-04 smallant2002
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    2020-11-29 guoyibin
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