TY  - JOUR
T1  - IGF-1 Protects Myocardial Cells from ROS Stress-Induced Apoptosis via Up-Regulating ARC
AU - Guo, DingZong AU - Zhu, Haibao AU - Liu, Dongyang AU - Wu, Liming AU - Xi, Zhaofang 
JO  - Journal of Animal and Veterinary Advances
VL  - 11
IS  - 11
SP  - 1901
EP  - 1906
PY  - 2012
DA  - 2001/08/19
SN  - 1680-5593
DO  - javaa.2012.1901.1906
UR  - https://makhillpublications.co/view-article.php?doi=javaa.2012.1901.1906
KW  - ARC
KW  -IGF-1
KW  -hydrogen peroxide
KW  -H9C2 cells
KW  -China
KW  -apoptosis
AB  - 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.
ER  -