Immune system-mediated atherosclerosis caused by deficiency of long non-coding RNA MALAT1 in ApoE-/-mice
Immune system-mediated atherosclerosis caused by deficiency of long non-coding RNA MALAT1 in ApoE-/-mice
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DOI：
10.1093/cvr/cvy202
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发表时间：
2019-02-01
影响因子：
10.8
通讯作者：
Poller, Wolfgang
中科院分区：
文献类型：
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作者：
Gast, Martina;Rauch, Bernhard H.;Poller, Wolfgang
免疫系统被认为是动脉粥样硬化的关键驱动因素，除了蛋白质和microRNAs (miRs)，长链非编码rna （lncRNAs）也参与免疫控制。我们之前报道了lncRNA转移相关肺腺癌转录本1 （MALAT1）参与心肌炎模型的心脏先天免疫。在这里，我们研究了MALAT1缺乏对动脉粥样硬化发展的影响。方法与结果杂合子malat1缺陷ApoE（-/-）小鼠即使在正常饮食的情况下，也在2个月内出现大量免疫系统失调和动脉粥样硬化。主动脉斑块面积(P
Aims The immune system is considered a key driver of atherosclerosis, and beyond proteins and microRNAs (miRs), long non-coding RNAs (lncRNAs) are implicated in immune control. We previously described that lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) is involved in cardiac innate immunity in a myocarditis model. Here, we investigated the impact of MALAT1 deficiency upon atherosclerosis development.Methods and results Heterozygous MALAT1-deficient ApoE(-/-) mice displayed massive immune system dysregulation and atherosclerosis within 2 months even when kept on normal diet. Aortic plaque area (P