Clinical & Experimental Cardiology
Open Access

MITOL blocks mitochondrial dysfunction and cardiac cell death

5^th International Conference on Clinical & Experimental Cardiology

April 27-29, 2015 Philadelphia, USA

Peifeng Li, Jing Wang, Lynn Htet Htet Aung and Jinling Li

Posters-Accepted Abstracts: J Clin Exp Cardiolog

Abstract :

Myocardial infarction (MI) is one of the leading causes of death in the United States. Several studies have shown that apoptosis is the major process of cardiomyoctye loss during MI. Cardiomyocytes are enriched with mitochondria. The balance between mitochondrial fission and fusion regulates the mitochondrial morphology and function. Excessive mitochondrial fission triggers the cells to undergo apoptosis. Therefore, controlling mitochondrial fission could reduce the cardiac cell loss during MI. Recently, the mitochondrial ubiquitin ligase MITOL, localized in the mitochondrial outer membrane, was reported to play an important role in the regulation of mitochondrial dynamic and apoptosis. However, its underlying mechanism remains uncertain. To understand the involvement of MITOL in cardiac cell apoptosis, HL-1 cardiomyocytes were treated with H2O2 or doxorubicin and MITOL expression was evaluated with immunoblotting. We found that MITOL was up-regulated and the cell underwent apoptosis under treatment. We noted that over-expression of MITOL decreased the percentage of cells with mitochondrial fission and apoptosis (analyzed by TUNEL staining) by reducing the Drp1 accumulation in mitochondria and caspase-3 and caspase-9 activation. Conversely, upon knockdown of MITOL, a higher percentage of cells underwent mitochondrial fission and apoptosis. These findings suggest that MITOL plays a protective role against cardiac apoptosis, and may serve as a potential therapeutic target in apoptosis-related cardiac diseases.