长链非编码 RNA-MALAT1 通过调控 miR-30a/beclin-1 通路影响心肌梗死。
LncRNA-MALAT1 influences myocardial infarction by regulating miR-30a/beclin-1 pathway.
机构信息
Department of Emergency, Wuxi People's Hospital Affiliated to Nanjing Medical University, Wuxi, China.
出版信息
Eur Rev Med Pharmacol Sci. 2020 Jan;24(2):885-892. doi: 10.26355/eurrev_202001_20073.
OBJECTIVE
Long non-coding ribonucleic acid-metastasis-associated lung adenocarcinoma transcript 1 (lncRNA-MALAT1) has been confirmed as a key factor involving in various physiological and pathological processes. The present study aims to investigate whether lncRNA-MALAT1 affects the process of myocardial infarction (MI) in rats by regulating the micro RNA (miR-30a)/Beclin-1 (BECN1) pathway.
MATERIALS AND METHODS
Twelve healthy male Sprague-Dawley rats were randomly selected and equally divided into sham-operation group and MI group. In MI group, a rat model of acute MI (AMI) was established by ligating the left anterior descending coronary artery. Rats in sham-operation group were set as the control. The messenger RNA (mRNA) expression levels of lncRNA-MALAT1, miR-30a, and BECN1 in the infarcted myocardial tissues were detected via real-time fluorescence quantitative polymerase chain reaction (qRT-PCR). The rat myocardial cell line H9c2 was cultured in vitro and then transfected with vectors of lncRNA-MALAT1, miR-30a, and BECN1. After that, qRT-PCR was performed to measure mRNA levels of lncRNA-MALAT1, miR-30a, and BECN1 in H9c2 cells. The protein level of BECN1 in cells was determined via Western blotting (WB) assay.
RESULTS
Expression levels of lncRNA-MALAT1 and BECN1 in the rat myocardium of MI group were up-regulated markedly (p<0.01), while miR-30a was down-regulated notably (p<0.01) compared with those in sham-operation group. After H9c2 cells were transfected with overexpression vectors of lncRNA-MALAT1 or miR-30a, expression levels of miR-30a (p<0.01) and BECN1 (p<0.01) were remarkably down-regulated, respectively.
CONCLUSIONS
LncRNA-MALAT1 up-regulates the expression of BECN1 by binding to miR-30a, thereby increasing the level of cell autophagy after MI.
目的
长链非编码核糖核酸-转移相关肺腺癌转录本 1（lncRNA-MALAT1）已被证实为参与多种生理和病理过程的关键因素。本研究旨在探讨 lncRNA-MALAT1 是否通过调节微小 RNA（miR-30a）/Beclin-1（BECN1）通路影响大鼠心肌梗死（MI）过程。
材料和方法
随机选取 12 只健康雄性 Sprague-Dawley 大鼠，均等分为假手术组和 MI 组。MI 组通过结扎左前降支冠状动脉建立急性心肌梗死（AMI）大鼠模型。假手术组大鼠设为对照组。采用实时荧光定量聚合酶链反应（qRT-PCR）检测梗死心肌组织中 lncRNA-MALAT1、miR-30a 和 BECN1 的信使 RNA（mRNA）表达水平。体外培养大鼠心肌细胞系 H9c2，然后转染 lncRNA-MALAT1、miR-30a 和 BECN1 载体。之后，采用 qRT-PCR 检测 H9c2 细胞中 lncRNA-MALAT1、miR-30a 和 BECN1 的 mRNA 水平。采用 Western blot（WB）法测定细胞中 BECN1 的蛋白水平。
结果
MI 组大鼠心肌组织中 lncRNA-MALAT1 和 BECN1 的表达水平显著上调（p<0.01），而 miR-30a 的表达水平显著下调（p<0.01），与假手术组相比。H9c2 细胞转染 lncRNA-MALAT1 或 miR-30a 的过表达载体后，miR-30a（p<0.01）和 BECN1（p<0.01）的表达水平分别显著下调。
结论
lncRNA-MALAT1 通过与 miR-30a 结合上调 BECN1 的表达，从而增加 MI 后细胞自噬水平。
Zotero 插件