Journal of Animal and Veterinary Advances
ISSN: Online 1993-601XISSN: Print 1680-5593
Abstract
Insulin-like Growth Factor-1 (IGF-1) and Apoptosis Repressor with Caspase recruitment domain (ARC) play an important role in regulating apoptosis. Although, the precise mechanisms of IGF-1 and ARC in this process have not been defined, they have similar anti-apoptotic effects in myocardial cells, suggesting that these effects are related. Researchers found that H2O2 can induce ARC reduction in H9C2 cells but IGF-1 can change this trend. To clarify this trend using immunofluorescence and immunoblot analysis, researchers found that LY294002 (PI3K inhibitor) blocked IGF-1 up-regulation of ARC protein and blocked the protective effect of IGF-1 on myocardial cell apoptosis induced by oxidative stress. These results indicate that IGF-1 up-regulates ARC protein expression via the PI3K pathway which protects against myocardial cell apoptosis induced by oxidative stress.
How to cite this article:
DingZong Guo, Haibao Zhu, Dongyang Liu, Liming Wu and Zhaofang Xi. IGF-1 Protects Myocardial Cells from ROS Stress-Induced Apoptosis via Up-Regulating ARC.
DOI: https://doi.org/10.36478/javaa.2012.1901.1906
URL: https://www.makhillpublications.co/view-article/1680-5593/javaa.2012.1901.1906