Cargando…

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...

Descripción completa

Detalles Bibliográficos
Autores principales: Qi, Jing Rui, Zhao, Dian Ru, Zhao, Li, Luo, Fan, Yang, Mei
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2021
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985160/
https://www.ncbi.nlm.nih.gov/pubmed/33768113
http://dx.doi.org/10.3389/fmolb.2020.621324
_version_ 1783668184363040768
author Qi, Jing Rui
Zhao, Dian Ru
Zhao, Li
Luo, Fan
Yang, Mei
author_facet Qi, Jing Rui
Zhao, Dian Ru
Zhao, Li
Luo, Fan
Yang, Mei
author_sort Qi, Jing Rui
collection PubMed
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.
format Online
Article
Text
id pubmed-7985160
institution National Center for Biotechnology Information
language English
publishDate 2021
publisher Frontiers Media S.A.
record_format MEDLINE/PubMed
spelling pubmed-79851602021-03-24 MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice Qi, Jing Rui Zhao, Dian Ru Zhao, Li Luo, Fan Yang, Mei Front Mol Biosci Molecular Biosciences 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. Frontiers Media S.A. 2021-03-09 /pmc/articles/PMC7985160/ /pubmed/33768113 http://dx.doi.org/10.3389/fmolb.2020.621324 Text en Copyright © 2021 Qi, Zhao, Zhao, Luo and Yang. http://creativecommons.org/licenses/by/4.0/ This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.
spellingShingle Molecular Biosciences
Qi, Jing Rui
Zhao, Dian Ru
Zhao, Li
Luo, Fan
Yang, Mei
MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice
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 Molecular Biosciences
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7985160/
https://www.ncbi.nlm.nih.gov/pubmed/33768113
http://dx.doi.org/10.3389/fmolb.2020.621324
work_keys_str_mv AT qijingrui mir520a3pinhibitedmacrophagepolarizationandpromotedthedevelopmentofatherosclerosisviatargetinguvraginapolipoproteineknockoutmice
AT zhaodianru mir520a3pinhibitedmacrophagepolarizationandpromotedthedevelopmentofatherosclerosisviatargetinguvraginapolipoproteineknockoutmice
AT zhaoli mir520a3pinhibitedmacrophagepolarizationandpromotedthedevelopmentofatherosclerosisviatargetinguvraginapolipoproteineknockoutmice
AT luofan mir520a3pinhibitedmacrophagepolarizationandpromotedthedevelopmentofatherosclerosisviatargetinguvraginapolipoproteineknockoutmice
AT yangmei mir520a3pinhibitedmacrophagepolarizationandpromotedthedevelopmentofatherosclerosisviatargetinguvraginapolipoproteineknockoutmice