Analysis of the mechanism of liquiritigenin in promoting cardiomyocyte regeneration based on miRNA-34b-TIA-1-SG molecular network-mediated autophagy

IF 0.7 4区 材料科学 Q3 Materials Science
Jiadi Zheng, Naiyu Zheng, Meise Lin
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引用次数: 0

Abstract

This study aims to clarify that miRNA-34b affects the autophagy through regulating TIA-1-SG and explore the role of miRNA-34b-TIA-1-SG molecular network-mediated autophagy in cardiomyocyte regeneration. 32 patients with autophagy injury caused by myocardial ischemia perfusion admitted to the hospital were included and 32 healthy controls were enrolled at the same time. ELISA was used to detect miRNA-34b level. Cardiomyocytes were isolated and cultured by adherence method and the relationship between miRNA-34b and TIA-1-SG was analyzed by dual-luciferase gene reporter assay. The correlation between myocardial autophagy and liquiritigenin treatment was assessed along with qRT-PCR analysis of the changes of genes (TIA-1, SG, ULK1, OsATG7, FAM176A, Beclin 1). miRNA-34b expression in 32 patients with myocardial autophagy injury was higher than normal group. miRNA-34b binds to the 3′-UTR of TIA-1 and transfection of miRNA-34b inhibitor increased the luciferase activity, which was not affected in pMIR-TIA-1-mut group, confirming the relationship between miRNA-34b and TIA-1. The addition of liquiritigenin can promote the reduction of expression of myocardial autophagy injury-related genes. In the absence of liquiritigenin, the expression of genes related to myocardial autophagy injury increased significantly. Autophagy imbalance plays an important role in myocardial infarction, which participates in myocardial infarction. miRNA-34b can target and regulate TIA-1 gene, promote myocardial infarction repair, and inhibit the state of autophagy by regulating autophagy-related gene TIA-1. Liquiritigenin regulates autophagy imbalance in myocardial infarction to delay myocardial remodeling and improve prognosis.
基于miRNA-34b-TIA-1-SG分子网络介导的自噬分析利尿原素促进心肌细胞再生的机制
本研究旨在阐明miRNA-34b通过调控TIA-1-SG影响自噬,探讨miRNA-34b-TIA-1-SG分子网络介导的自噬在心肌细胞再生中的作用。纳入本院收治的32例心肌缺血灌注所致自噬损伤患者,同时纳入32例健康对照。ELISA法检测miRNA-34b水平。采用贴壁法分离培养心肌细胞,采用双荧光素酶基因报告基因法分析miRNA-34b与TIA-1-SG的关系。通过qRT-PCR分析心肌自噬与利尿原素治疗的相关性(TIA-1、SG、ULK1、OsATG7、FAM176A、Beclin 1)。32例心肌自噬损伤患者的miRNA-34b表达高于正常组。miRNA-34b与TIA-1的3′-UTR结合,转染miRNA-34b抑制剂可提高荧光素酶活性,而pMIR-TIA-1-mut组荧光素酶活性不受影响,证实了miRNA-34b与TIA-1之间的关系。利尿原的加入可促进心肌自噬损伤相关基因表达的降低。在缺乏利尿原的情况下,心肌自噬损伤相关基因的表达明显增加。自噬失衡在心肌梗死中起重要作用,参与心肌梗死的发生。miRNA-34b可通过调控自噬相关基因TIA-1靶向调控TIA-1基因,促进心肌梗死修复,抑制自噬状态。利尿原调节心肌梗死自噬失衡,延缓心肌重构,改善预后。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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来源期刊
Materials Express
Materials Express NANOSCIENCE & NANOTECHNOLOGY-MATERIALS SCIENCE, MULTIDISCIPLINARY
自引率
0.00%
发文量
69
审稿时长
>12 weeks
期刊介绍: Information not localized
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