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    ASIA unversity > 醫學暨健康學院 > 期刊論文 >  Item 310904400/6772


    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/6772


    Title: Hypoxia-induced compensatory effect as related to Shh and HIF-1α in ischemia embryo rat heart
    Authors: Hwang, Jin-Ming;Weng, Yi-Jiun;Lin, Tzu-En;Da-Tian Bau;Ko, Fu-Yang;Fuu-Jen Tsai;Chang-Hai Tsai;Chieh-Hsi Wu;Lin, Pei-Cheng;Chih-Yang Huang;Wei-Wen Kuo
    Date: 2008-04
    Issue Date: 2009-12-23 14:22:11 (UTC+8)
    Publisher: Asia University
    Abstract: Chronic cardiac ischemia/hypoxia induces coronary collateral formation and cardiomyocyte proliferation. Hypoxia can induce cellular adaptive responses, such as synthesis of VEGF for angiogenesis and IGF-2 for proliferation. Both reduce apoptotic effects to minimize injury or damage. To investigate the mechanism of neoangiogenesis and proliferation of fetal heart under umbilical cord compression situation, we used H9c2 cardiomyoblast cell culture, and in vivo embryonic hearts as our study models. Results showed hypoxia induced not only the increase of IGF-2 and VEGF expression but also the activation of their upstream regulatory genes, HIF-1α and Shh. The relationship between HIF-1α and Shh was further studied by using cyclopamine and 2-ME2, inhibitor of Shh and HIF-1α signaling, respectively, in the cardiomyoblast cell culture under hypoxia. We found that the two inhibitors not only blocked their own signal pathway, but also inhibited each other. The observations revealed when fetal heart under hypoxia that HIF-1α and Shh pathways maybe involve in cell proliferation and neoangiogenesis to minimize injury or damage, whereas the complex cross-talk between the two pathways remains unknown.
    Relation: MOLECULAR AND CELLULAR BIOCHEMISTRY 311 (1-2): 179-187
    Appears in Collections:[醫學暨健康學院] 期刊論文

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