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Título: | LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury |
Fecha de publicación: | 2021 |
Editorial: | Universidad de Murcia, Departamento de Biologia Celular e Histiologia |
Cita bibliográfica: | Histology and Histopathology Vol. 36, nº12 (2021) |
ISSN: | 0213-3911 1699-5848 |
Materias relacionadas: | CDU::6 - Ciencias aplicadas::61 - Medicina::616 - Patología. Medicina clínica. Oncología |
Palabras clave: | LncRNA TUG1 Myocardial ischemia reperfusion injury Apoptosis |
Resumen: | 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 |
Autor/es principal/es: | Fu, Dongliang Gao, Tong Liu, Mengru Li, Chunyan Li, Haiwei Jiang, Hong Li, Xianlun |
URI: | http://hdl.handle.net/10201/128105 |
DOI: | https://doi.org/10.14670/HH-18-381 |
Tipo de documento: | info:eu-repo/semantics/article |
Número páginas / Extensión: | 12 |
Derechos: | info:eu-repo/semantics/openAccess Attribution-NonCommercial-NoDerivatives 4.0 Internacional |
Aparece en las colecciones: | Vol.36,nº12 (2021) |
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Fu-36-1261-1272-2021.pdf | 5,11 MB | Adobe PDF | Visualizar/Abrir |
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