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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/8383

    Title: Enhancement of AG1024-Induced H9c2 Cardiomyoblast Cell Apoptosis via the Interaction of IGF2R with G alpha Proteins and Its Downstream PKA and PLC-beta Modulators by IGF-II
    Authors: Chu, CH;Chu, Chun-Hsien;Huang, CY;Huang, Chih-Yang;Lu, MC;Lu, Ming-Chin;Lin, JA;Lin, James A.;Tsai, FJ;Tsai, Fuu-Jen;Tsai, CH;Tsai, Chang-Hai;Chu, CY;Chu, Chia-Yih;Kuo, VH;Kuo, Wu-Hsien;Chen, LM;Chen, Li-Mien;Chen, LY;Chen, Ling-Yun
    Contributors: 保健系
    Date: 2009-02
    Issue Date: 2010-03-26 10:46:17 (UTC+8)
    Publisher: Asia University
    Abstract: Our previous studies found that insulin-like growth factor-1 receptor (IGF1R) signaling blockade caused cardiac hypertrophy, and that apoptosis is required for upregulating the IGF-II and the IGF-II/mannose 6-phosphate receptor (IGF2R) gene. However, the role of IGF-II in the regulation of cell apoptosis through IGF2R is little known. In this study, we hypothesized that IGF-II may induce cell apoptosis through IGF2R but is dependent on IGF1R activity. Western blots and TUNEL assay revealed that in the presence of IGF1R, exogenous IGF-II acts, like IGF-I, would increase phospho-Akt through IGF1R, but does not affect the caspase 3 activation and apoptotic induction in H9c2 cardiomyoblast cells. Conversely, AG1024, an inhibitor of IGF1R activity, causes cell apoptosis, and the treatment with IGF-II further enhances this process, implying that it occurs through IGF2R. Moreover, immunoprecipitation assay revealed that treatment with IGF-II could enhance the interaction of IGF2R with G alpha i and G alpha q but reduce its binding with G alpha s, resulting in the reduction of phospho-PKA and the activation of PLC-beta. Taken together, these data provide new insight into the dual role of IGF-II in the control of IGF1R dependent cell apoptosis and involved activation of IGF2R signaling. Improving IGF1R activity and suppressing IGF2R may be a good strategy to prevent the progression of heart disease with cardiomyocyte apoptosis.
    Relation: CHINESE JOURNAL OF PHYSIOLOGY, 52(1):31-37.
    Appears in Collections:[食品營養與保健生技學系] 期刊論文

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