LncRNA TUG1 aggravates cardiomyocyte apoptosis and myocardial ischemia/reperfusion injury

• Dongliang Fu ^[1] ; Tong Gao ^[1] ; Mengru Liu ^[1] ; Chunyan Li ^[1] ; Haiwei Li ^[1] ; Hong Jiang ^[1] ; Xianlun Li ^[1]
  1. [1] China-Japan Friendship Hospital

     China-Japan Friendship Hospital

     China

     
• Localización: Histology and histopathology: cellular and molecular biology, ISSN-e 1699-5848, ISSN 0213-3911, Vol. 36, Nº. 12, 2021, págs. 1261-1272
• Idioma: inglés
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• 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 may have therapeutic effects in treating MI/R injury.