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    Please use this identifier to cite or link to this item: http://asiair.asia.edu.tw/ir/handle/310904400/16257


    Title: Hypoxia-induced compensatory effect as related to Shh and HIF-1a in ischemia embryo rat heart
    Authors: Jin-Ming Hwang;Yi-Jiun Weng;James A. Lin;Da-Tian Bau;Fu-Yang Ko;Fuu-Jen Tsai;Chang-Hai Tsai;Chieh-Hsi Wu;Pei-Cheng Lin;Chih-Yang Huang;Wei-Wen Kuo
    Contributors: 生物科技學系
    Date: 2008-01
    Issue Date: 2012-11-23 17:10:35 (UTC+8)
    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-1alpha and Shh. The relationship between HIF-1alpha and Shh was further studied by using cyclopamine and 2-ME2, inhibitor of Shh and HIF-1alpha 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-1alpha 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):179-87.
    Appears in Collections:[生物科技學系] 期刊論文

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