Hyperphosphate-Induced Myocardial Hypertrophy through the GATA-4/NFAT-3 Signaling Pathway Is Attenuated by ERK Inhibitor Treatment

doi:10.1159/000371454

中山醫學大學機構典藏 CSMUIR > 醫學科技學院 > 醫學檢驗暨生物技術學系暨碩士班 > 期刊論文 > Item 310902500/17907

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题名:	Hyperphosphate-Induced Myocardial Hypertrophy through the GATA-4/NFAT-3 Signaling Pathway Is Attenuated by ERK Inhibitor Treatment
作者:	Liu, Yao-Lung Huang, Chiu-Ching Chang, Chiz-Chung Chou, Che-Yi Lin, Shih-Yi Wang, I-Kuan Hsieh, Dennis Jine-Yuan Jong, Gwo-Ping Huang, Chih-Yang Wang, Chao-Min
贡献者:	中山醫大
关键词:	Hyperphosphate;Cardiomyocyte hypertrophy;Calcineurin;ERK inhibitor
日期:	2015
上传时间:	2017-07-04T08:22:45Z (UTC)
出版者:	Cardiorenal Med
ISSN:	1664-3828
摘要:	Abstract Background/Aims Numerous epidemiological studies have associated elevated serum phosphorus levels with cardiovascular disease and the risk of death in the general population as well as in chronic kidney disease (CKD) and dialysis patients. In this study, we explored whether elevated phosphate conditions induce cardiac hypertrophy and attempted to identify the molecular and cellular mechanisms in the hypertrophic response. Methods H9c2 myocardial cells were incubated in high-phosphate conditions to induce hypertrophy. Pathological hypertrophic responses were measured in terms of cell size, arrangement of actin filaments, and hypertrophy markers such as atrial natriuretic peptide (ANP) and B-type natriuretic peptide (BNP) in myocardial cells. Several transcriptional factors involved in cardiac hypertrophy development were measured to investigate the molecular pathways involved in elevated phosphate-induced cardiac hypertrophy. Results High-phosphate conditions induced cellular hypertrophy, marked by increased cell size, reorganization of actin filaments, and upregulation of both ANP and BNP in H9c2 cells. Both upstream calcineurin and downstream transcription factors, including GATA-4 and NFAT-3, were significantly increased under hyperphosphate conditions. Moreover, both MEK1/2 and ERK1/2 expression increased significantly, and cellular hypertrophy was markedly attenuated by U0126, an ERK1/2 inhibitor. Conclusions These results suggest that hyperphosphate conditions induce myocardial hypertrophy through the ERK signaling pathway in H9c2 cells. Our findings provide a link between the hyperphosphate-induced response and the ERK/NFAT-3 signaling pathway that mediates the development of cardiac hypertrophy. In view of the potent and selective activity of the ERK inhibitor U0126, this agent warrants further investigation as a candidate for preventing hyperphosphate-induced cardiac hypertrophy in CKD and dialysis patients.
URI:	http://dx.doi.org/10.1159/000371454 https://ir.csmu.edu.tw:8080/ir/handle/310902500/17907
關聯:	Cardiorenal Med. 2015 Apr; 5(2): 79–88.
显示于类别:	[醫學檢驗暨生物技術學系暨碩士班] 期刊論文

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