IGF-II receptor signaling induced cell hypertrophy and ANP/BNP expression via Gαq interaction and PKCα/ CaMKII activation in the H9c2 cardiomyoblast cells

中國醫藥大學機構典藏 China Medical University Repository, Taiwan > 醫學院 > 基礎醫學研究所 > 期刊論文 > Item 310903500/7024

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题名:	IGF-II receptor signaling induced cell hypertrophy and ANP/BNP expression via Gαq interaction and PKCα/ CaMKII activation in the H9c2 cardiomyoblast cells
作者:	(Chu Chun-Hsien);(Tzang Bor-Show);(Chen Li-Mien);(Kua Chia-Hua);(Cheng Yi-Chang);(Chen Ling-Yun);蔡輔仁(Fuu-Jen Tsai);蔡長海(Chang-Hai Tsai);郭薇雯(Wei-Wen Kuo);黃志揚(Chih-Yang Huang)
贡献者:	醫學院基礎醫學研究所
日期:	2008-01
上传时间:	2009-08-26 16:09:43 (UTC+8)
摘要:	The role played by IGF-II in signal transduction through the IGF-II/mannose-6-phosphate receptor (IGF2R) in heart tissue has been poorly understood. In our previous studies, we detected an increased expression of IGF-II and IGF2R in cardiomyocytes that had undergone pathological hypertrophy. We hypothesized that after binding with IGF-II, IGF2R may trigger intracellular signaling cascades involved in the progression of pathologically cardiac hypertrophy. In this study, we used immunohistochemical analysis of the human cardiovascular tissue array to detect expression of IGF2R. In our study of H9c2 cardiomyoblast cell cultures, we used the rhodamine phalloidin staining to measure the cell hypertrophy and western blot to measure the expression of cardiac hypertrophy markers atrial natriuretic peptide (ANP) and brain natriuretic peptide (BNP) in cells treated with IGF-II. We found that a significant association between IGF2R overexpression and myocardial infarction. The treatment of H9c2 cardiomyoblast cells with IGF-II not only induced cell hypertrophy but also increased the protein level of ANP and BNP. Using Leu27IGF-II, an analog of IGF-II which interacts selectively with the IGF2R, to specifically activate IGF2R signaling cascades, we found that binding of Leu27IGF-II to IGF2R led to an increase in the phosphorylation of protein Kinase C (PKC)-{alpha} and calcium/calmodulin-dependent protein kinase II (CaMKII) in a G{alpha}q-dependent manner. By the inhibition of PKC-{alpha}/CaMKII activity, we found that IGF-II and Leu27IGF-II-induced cell hypertrophy and upregulation of ANP and BNP were significantly suppressed. Taken together, this study provides a new insight into the effects of the IGF2R and its downstream signaling in cardiac hypertrophy. The suppression of IGF2R signaling pathways may be a good strategy to prevent the progression of pathological hypertrophy.
關聯:	JOURNAL OF ENDOCRINOLOGY 197(0)1 ~11
显示于类别:	[基礎醫學研究所] 期刊論文

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