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miRNA-150 靶向 PU.1 并调节实验性自身免疫性脑脊髓炎中的巨噬细胞分化和功能。

MicroRNA-150 targets PU.1 and regulates macrophage differentiation and function in experimental autoimmune encephalomyelitis.

机构信息

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Shefa Neuroscience Research Center, Khatam Alanbia Hospital, Tehran, Iran.

Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran.

出版信息

J Neuroimmunol. 2018 Oct 15;323:167-174. doi: 10.1016/j.jneuroim.2018.06.010. Epub 2018 Jun 22.

Abstract

PU.1 is a transcription factor which is expressed in myeloid cells. Herein, we investigated the expression of PU.1 and its potentially targeting miRNAs in the central nervous system (CNS) of mice with experimental autoimmune encephalitis (EAE) and in cultured primary macrophages. PU.1 levels where highly induced in EAE spinal cords and in activated macrophages; this was associated with a significant reduction in miR-150-5p levels at chronic phase of disease and in activated cells. Luciferase assays confirmed the PU.1-miR-150-5p interaction. Overexpression of miR-150-5p in macrophages decreased the expression of proinflammatory cytokines and shifted the polarization of macrophages away from the M1-like phenotype.

摘要

PU.1 是一种在髓系细胞中表达的转录因子。在此,我们研究了实验性自身免疫性脑脊髓炎 (EAE) 小鼠中枢神经系统 (CNS) 和原代培养巨噬细胞中 PU.1 的表达及其潜在的靶向 microRNA。EAE 脊髓和激活的巨噬细胞中高度诱导了 PU.1 水平;这与疾病慢性期和激活细胞中 miR-150-5p 水平的显著降低有关。荧光素酶测定证实了 PU.1-miR-150-5p 相互作用。巨噬细胞中 miR-150-5p 的过表达降低了促炎细胞因子的表达,并使巨噬细胞的极化远离 M1 样表型。

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