Functional analysis of ceRNA network of lncRNA TSIX/miR-34a-5p/RBP2 in acute myocardial infarction based on GEO database

The identification of innovative gene biomarkers with clinical efficacy is warranted for the treatment of acute myocardial infarction (AMI). The current study sought to screen potential target genes in AMI via bioinformatic analysis and analyze their effects on cardiomyocyte apoptosis. The different...

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Autores principales: Jiezhong Lin, Jianyi Zhou, Guiting Xie, Xiongwei Xie, Yanfang Luo, Jinguang Liu
Formato: article
Lenguaje:EN
Publicado: Taylor & Francis Group 2021
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Acceso en línea:https://doaj.org/article/2670126080c24e209e68ce793b8089c9
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Sumario:The identification of innovative gene biomarkers with clinical efficacy is warranted for the treatment of acute myocardial infarction (AMI). The current study sought to screen potential target genes in AMI via bioinformatic analysis and analyze their effects on cardiomyocyte apoptosis. The differentially expressed long non-coding RNAs (lncRNAs) of AMI were screened, and the downstream microRNAs (miRNAs) and mRNAs of lncRNA antisense for X-inactive-specific transcript (lncRNA TSIX) were predicted accordingly. The diagnostic relationship between the 12 differentially expressed lncRNAs and AMI was analyzed by receiver operating characteristic (ROC). Next, the expressions of 12 lncRNAs, including miR-34a-5p and retinol binding protein 2 (RBP2) were all detected. The targeting relationships of miR-34a-5p with lncRNA TSIX and RBP2 were verified. AMI model was established and treated with Ad-TSIX and/or agomiR-34a-5p to evaluate the cardiac function and cardiomyocyte apoptosis of AMI mice. LncRNA TSIX was identified as the most differentially expressed lncRNA in AMI. Our findings revealed that LncRNA TSIX could function as an AMI diagnostic marker. LncRNA TSIX could target miR-34a-5p and miR-34a-5p could target RBP2. Upregulation of lncRNA TSIX could ameliorate cardiac injury inflicted by AMI and mitigate cardiomyocyte apoptosis. Upregulation of miR-34a-5p reversed the effect of lncRNA TSIX overexpression to ameliorate cardiomyocyte apoptosis in AMI mice. Overall, the overexpression of lncRNA TSIX inhibits cardiomyocyte apoptosis by competing with RBP2 to bind to miR-34a-5p and promoting RBP2.