Publication:
LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury

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Fu-36-1261-1272-2021.pdf(4.99 MB)
Date
2021
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Authors
Fu, Dongliang ; Gao, Tong ; Liu, Mengru ; Li, Chunyan ; Li, Haiwei ; Jiang, Hong ; Li, Xianlun
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Publisher
Universidad de Murcia, Departamento de Biologia Celular e Histiologia
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DOI
https://doi.org/10.14670/HH-18-381
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info:eu-repo/semantics/article
Description
Abstract
Cardiomyocyte apoptosis is a fundamental pathogenic factor leading to myocardial ischemia/ reperfusion (MI/R) injury. The long non-coding RNA (lncRNA) TUG1 regulates apoptosis in various cell types. We report here that TUG1 expression is induced in mouse heart following MI/R injury as well as in cardiomyocytes subjected to simulated ischemia/ reperfusion (SI/R) in vitro. Clinically, TUG1 expression is also elevated in plasma from patients with acute myocardial infarction (AMI), which implies its potential application as a disease biomarker. Functionally, TUG1 overexpression promotes, and its knockdown reduces SI/R-induced lactate dehydrogenase (LDH) release and caspase-3 activity in cardiomyocytes in vitro, illustrating that TUG1 exacerbates SI/R-induced apoptosis. Furthermore, in vivo, TUG1 aggravates MI/R injury in a mouse model, and subsequent observations show concurrent increased apoptosis of cardiomyocytes. Hence, this study unveils a clinical relevance and functional role of TUG1 in MI/R injury, and also implicates that targeting TUG1 m
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LncRNA , TUG1 , Myocardial ischemia , reperfusion injury , Apoptosis
Citation
Histology and Histopathology Vol. 36, nº12 (2021)
URI
http://hdl.handle.net/10201/128105
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Histology and histopathology Vol.36,nº12 (2021)
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