Please use this identifier to cite or link to this item:
標題: Hypoxia-induced compensatory effect as related to Shh and HIF-1 alpha in ischemia embryo rat heart
作者: Hwang, J.M.
Weng, Y.J.
Lin, J.A.
Bau, D.T.
Ko, F.Y.
Tsai, F.J.
Tsai, C.H.
Wu, C.H.
Lin, P.C.
Huang, C.Y.
Kuo, W.W.
關鍵字: H9c2 cells;Shh;HIF-1 alpha;hypoxia;ischemia;inducible factor 1-alpha;growth-factor-i;human prostate-cancer;tumor;angiogenesis;gene-expression;sonic hedgehog;insulin;pathway;apoptosis;injury
Project: Molecular and Cellular Biochemistry
期刊/報告no:: Molecular and Cellular Biochemistry, Volume 311, Issue 1-2, Page(s) 179-187.
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-1 alpha and Shh. The relationship between HIF-1 alpha and Shh was further studied by using cyclopamine and 2-ME2, inhibitor of Shh and HIF-1 alpha 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-1 alpha 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.
ISSN: 0300-8177
DOI: 10.1007/s11010-008-9708-6
Appears in Collections:期刊論文

Show full item record

Google ScholarTM




Items in DSpace are protected by copyright, with all rights reserved, unless otherwise indicated.