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International Journal of Pharmacology

Year: 2019 | Volume: 15 | Issue: 4 | Page No.: 503-508
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Authors

Dongyun Yin

Qilin Wan

Qunhui Ye

Yongzhi Deng

Bin Lin

Bin Lin

Lin Wu

Lin Wu

Keywords

Research Article

Cardiomyocyte Hypertrophy induced by Visfatin in H9c2 Embryonic Rat Cardiac Cells via ERK1/2 Signaling Pathway

Dongyun Yin, Qilin Wan, Qunhui Ye, Yongzhi Deng, Bin Lin Bin Lin's LiveDNA and Lin Wu Lin Wu's LiveDNA
Background and Objective: Visfatin is an adipokine which is abundantly expression in visceral adipose tissue. It has insulin-like effect and hypoglycemic effect. Visfatin can induce the production of inflammatory factors and myocardial hypertrophy but the exact molecular mechanisms remain unclear. The purpose of this study was to investigate the underlying molecular mechanism that visfatin induces cardiomyocyte hypertrophy. Materials and Methods: H9c2 cells were cultured and treated with visfatin. Cell surface area was measured with ImageJ software. Protein synthesis was calculated by dividing the protein content by the cell number. BNP, α-SMA, p-ERK1/2 and ERK1/2 protein expression were detected by Western blotting. Results: The results showed that visfatin induced cell surface area, protein synthesis, BNP, α-SMA and p-ERK1/2 protein expression increase significantly. Pre-treatment with MAPK Kinase Inhibitor PD98059 of ERK1/2 signaling pathway significantly attenuated these effects of visfatin. Conclusion: The results suggested that visfatin induces cardiomyocyte hypertrophy through the activation of ERK1/2 signaling pathway.
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