MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice

Atherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNA...

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Main Authors: Jing Rui Qi, Dian Ru Zhao, Li Zhao, Fan Luo, Mei Yang
Format: Article
Language:English
Published: Frontiers Media S.A. 2021-03-01
Series:Frontiers in Molecular Biosciences
Subjects:
Online Access:https://www.frontiersin.org/articles/10.3389/fmolb.2020.621324/full
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author Jing Rui Qi
Dian Ru Zhao
Li Zhao
Fan Luo
Mei Yang
author_facet Jing Rui Qi
Dian Ru Zhao
Li Zhao
Fan Luo
Mei Yang
author_sort Jing Rui Qi
collection DOAJ
description Atherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNAs) are involved in the process of AS. However, the pathway and gene miRNAs targeting are poorly understood. Here we reported that miR-520a-3p was increased in mice with AS and silencing of miR-520a-3p attenuated AS process. Furthermore, inhibition of miR-520a-3p increased the expression of α-SMA and collagen. In addition, miR-520a-3p silencing inhibited the expression of M1 macrophage polarization markers and pro-inflammatory genes and promoted the M2 macrophage polarization. What’s more, forced expression of miR-520a-3p diminished IL4/IL13 induced macrophage autophagy via targeting UVRAG. Collectively, our study reveals the role of miR-520a-3p in macrophage polarization and suggests the potential of miRNA as a novel treatment target of AS.
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spelling doaj.art-22234084786543cc98269542d05d88542022-12-21T21:31:33ZengFrontiers Media S.A.Frontiers in Molecular Biosciences2296-889X2021-03-01710.3389/fmolb.2020.621324621324MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout MiceJing Rui Qi0Dian Ru Zhao1Li Zhao2Fan Luo3Mei Yang4Department of Geratology, Cangzhou Central Hospital, Cangzhou, ChinaXinxiang Medical University, Xinxiang, ChinaDepartment of Geratology, Cangzhou Central Hospital, Cangzhou, ChinaDepartment of Geratology, Cangzhou Central Hospital, Cangzhou, ChinaDepartment of Geratology, Cangzhou Central Hospital, Cangzhou, ChinaAtherosclerosis (AS), a kind of chronic inflammatory blood vessel disease, is a main cause of cardiovascular disease, which is a leading cause of mortality around the world. Accumulation of macrophages induced by inflammation contributes to AS development. It has been indicated that microRNAs (miRNAs) are involved in the process of AS. However, the pathway and gene miRNAs targeting are poorly understood. Here we reported that miR-520a-3p was increased in mice with AS and silencing of miR-520a-3p attenuated AS process. Furthermore, inhibition of miR-520a-3p increased the expression of α-SMA and collagen. In addition, miR-520a-3p silencing inhibited the expression of M1 macrophage polarization markers and pro-inflammatory genes and promoted the M2 macrophage polarization. What’s more, forced expression of miR-520a-3p diminished IL4/IL13 induced macrophage autophagy via targeting UVRAG. Collectively, our study reveals the role of miR-520a-3p in macrophage polarization and suggests the potential of miRNA as a novel treatment target of AS.https://www.frontiersin.org/articles/10.3389/fmolb.2020.621324/fullMiR-520a-3pmacrophage polarizationautophagyatherosclerosischronic inflammatory blood vessel disease
spellingShingle Jing Rui Qi
Dian Ru Zhao
Li Zhao
Fan Luo
Mei Yang
MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
Frontiers in Molecular Biosciences
MiR-520a-3p
macrophage polarization
autophagy
atherosclerosis
chronic inflammatory blood vessel disease
title MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
title_full MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
title_fullStr MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
title_full_unstemmed MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
title_short MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
title_sort mir 520a 3p inhibited macrophage polarization and promoted the development of atherosclerosis via targeting uvrag in apolipoprotein e knockout mice
topic MiR-520a-3p
macrophage polarization
autophagy
atherosclerosis
chronic inflammatory blood vessel disease
url https://www.frontiersin.org/articles/10.3389/fmolb.2020.621324/full
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