Hypoxia-induced compensatory effect as related to Shh and HIF-1α in ischemia embryo rat heart

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

研究成果: 雜誌貢獻文章同行評審

37 引文 斯高帕斯(Scopus)

摘要

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.

原文英語
頁(從 - 到)179-187
頁數9
期刊Molecular and Cellular Biochemistry
311
發行號1-2
DOIs
出版狀態已發佈 - 4月 2008
對外發佈

ASJC Scopus subject areas

  • 分子生物學
  • 臨床生物化學
  • 細胞生物學

指紋

深入研究「Hypoxia-induced compensatory effect as related to Shh and HIF-1α in ischemia embryo rat heart」主題。共同形成了獨特的指紋。

引用此