Author: Chen Wei-Kung Kuo Wei-Wen Hsieh Dennis Jine-Yuan Chang Hsin-Nung Pai Pei-Ying Lin Kuan-Ho Pan Lung-Fa Ho Tsung-Jung Viswanadha Vijaya Padma Huang Chih-Yang
Publisher: MDPI
E-ISSN: 1422-0067|16|11|27921-27930
ISSN: 1422-0067
Source: International Journal of Molecular Sciences, Vol.16, Iss.11, 2015-11, pp. : 27921-27930
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Abstract
During hypoxia, gene expression is altered by various transcription factors. Insulin-like growth factor-II (IGF2) is known to be induced by hypoxia, which binds to IGF2 receptor IGF2R that acts like a G protein-coupled receptor, might cause pathological hypertrophy or activation of the mitochondria-mediated apoptosis pathway. Cyclic adenosine monophosphate (cAMP) responsive element-binding protein (CREB) is central to second messenger-regulated transcription and plays a critical role in the cardiomyocyte survival pathway. In this study, we found that IGF2R level was enhanced in H9c2 cardiomyoblasts exposed to hypoxia in a time-dependent manner but was down-regulated by CREB expression. The over-expression of CREB in H9c2 cardiomyoblasts suppressed the induction of hypoxia-induced IGF2R expression levels and reduced cell apoptosis. Gel shift assay results further indicated that CREB binds to the promoter sequence of
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