@article{MAKHILLJAVA201211113484,
    title = {IGF-1 Protects Myocardial Cells from ROS Stress-Induced Apoptosis via Up-Regulating ARC},
    journal = {Journal of Animal and Veterinary Advances},
    volume = {11},
    number = {11},
    pages = {1901-1906},
    year = {2012},
    issn = {1680-5593},
    doi = {javaa.2012.1901.1906},
    url = {https://makhillpublications.co/view-article.php?issn=1680-5593&doi=javaa.2012.1901.1906},
    author = {DingZong,Haibao,Dongyang,Liming and},
    keywords = {ARC,IGF-1,hydrogen peroxide,H9C2 cells,China,apoptosis},
    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 H<SUB>2</SUB>O<SUB>2</SUB> 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.}
    }