LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury

xlomafota13 shared this article with you from Inoreader LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury Via Cellular and Molecular Biology Histol Histopathol. 2021 Oct 20:18381. doi: 10.14670/HH-18-381. Online ahead of print. ABSTRACT Cardiomyocyte apoptosis is a fundamental pathogenic factor leading to myocardial ischemia/reperfusion (MI/R) injury. The long non-coding RNA (IncRNA) 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 subsequ ent 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 may have therapeutic effects in treating MI/R injury. PMID:34668176 | DOI:10.14670/HH-18-381 View on the web Inoreader. Take back control of your news feed. Follow us on Twitter and Facebook.