MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice.
MiR-520a-3p Inhibited Macrophage Polarization and Promoted the Development of Atherosclerosis via Targeting UVRAG in Apolipoprotein E Knockout Mice.
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DOI：
10.3389/fmolb.2020.621324
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发表时间：
2020
影响因子：
5
通讯作者：
Yang M
中科院分区：
文献类型：
--
作者：
Qi JR;Zhao DR;Zhao L;Luo F;Yang M
动脉粥样硬化（Atheroplasty，AS）是一种慢性炎症性血管疾病，是心血管疾病的主要病因之一，也是世界范围内死亡率最高的疾病。炎症诱导的巨噬细胞积聚有助于AS的发展。已有研究表明microRNAs（miRNAs）参与了AS的发病过程。然而，通路和基因miRNA靶向知之甚少。我们在此报道了miR-520 a-3 p在AS小鼠中的表达增加，沉默miR-520 a-3 p可减弱AS的发生。抑制miR-520 a-3 p可增加α-SMA和胶原的表达。此外，miR-520 a-3 p沉默抑制M1巨噬细胞极化标志物和促炎基因的表达，促进M2巨噬细胞极化。此外，miR-520 a-3 p的强制表达通过靶向UVRAG减少了IL 4/IL 13诱导的巨噬细胞自噬。总的来说，我们的研究揭示了miR-520 a-3 p在巨噬细胞极化中的作用，并表明miRNA作为AS新治疗靶点的潜力。
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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影响因子：
30.5
作者：
Koelwyn GJ;Corr EM;Erbay E;Moore KJ
通讯作者：
Moore KJ
影响因子：
2.4
作者：
Bhaskaran M;Mohan M
通讯作者：
Mohan M
细胞特异性后通过微RNA对γ-核蛋白基因的转录调节。
影响因子：
3.7
作者：
Surgucheva I;Gunewardena S;Rao HS;Surguchov A
通讯作者：
Surguchov A
影响因子：
20.1
作者：
Tabas I;Bornfeldt KE
通讯作者：
Bornfeldt KE
影响因子：
5.6
作者：
Bi, Chang-Long;Zhang, Ying-Qi;Fu, Yi-Li
通讯作者：
Fu, Yi-Li