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Down-regulation of lncRNA MALAT1 alleviates vascular lesion and vascular remodeling of rats with hypertension

机译:lncRNA MALAT1的下调可减轻高血压大鼠的血管病变和血管重塑

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摘要

Objective: Recently, the effect of long non-coding RNAs (lncRNAs) in hypertension (HTN) has been identified. This study aims to explore the expression of lncRNA metastasis-associated lung adenocarcinoma transcript 1 (MALAT1) in HTN and its role in vascular lesion and remodeling of HTN rats.Results: LncRNA MALAT1 expression was up-regulated in HTN patients, and lncRNA MALAT1 could be an effective index of HTN diagnosis. Down-regulated MALAT1 and inhibited Notch-1 could reduce relative factor expression, including inflammation-related factors, endothelial function-related factors and oxidative stress-related factors, and inhibit apoptosis of aortic endothelial cells of HTN rats.Methods: LncRNA MALAT1 expression in HTN patients and healthy controls was detected by reverse transcription quantitative polymerase chain reaction (RT-qPCR). Angiotensin II (Ang II)-induced HTN rat models were injected with MALAT1-siRNA, empty lentivirus vector, Notch pathway inhibitor (DAPT) and dimethyl sulphoxide (DMSO) via caudal vein. After three-week treatment, changes of blood pressure, inflammatory factor levels, endothelial function-related factors, oxidative stress indices and apoptosis of vascular endothelial cells were determined by a series of assays.Conclusion: This study revealed that down-regulated lncRNA MALAT1 could alleviate the vascular lesion and remodeling of HTN rats, the mechanism may be related to the inhibited activation of Notch signaling pathway.
机译:目的:最近,人们已经确定了长非编码RNA(lncRNA)在高血压(HTN)中的作用。本研究旨在探讨lncRNA转移相关的肺腺癌转录本1(MALAT1)在HTN中的表达及其在HTN大鼠血管病变和重塑中的作用。结果:HTN患者LncRNA MALAT1表达上调,lncRNA MALAT1可能是诊断HTN的有效指标。下调MALAT1并抑制Notch-1可能降低炎症相关因子,内皮功能相关因子和氧化应激相关因子的相对表达,并抑制HTN大鼠主动脉内皮细胞凋亡。通过逆转录定量聚合酶链反应(RT-qPCR)检测HTN患者和健康对照。通过尾静脉向血管紧张素II(Ang II)诱导的HTN大鼠模型注射MALAT1-siRNA,空慢病毒载体,Notch途径抑制剂(DAPT)和二甲基亚砜(DMSO)。经过三周的治疗,通过一系列测定来测定血压,炎症因子水平,内皮功能相关因子,氧化应激指数和血管内皮细胞凋亡的变化。结论:本研究表明下调lncRNA MALAT1可能减轻HTN大鼠的血管病变和重塑,其机制可能与Notch信号通路激活受抑制有关。

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