BMP4 Induces Cardiomyocyte Hypertrophy Through the Activation of ERK 1/2 Signaling Pathway in H9c2 Cells

被引:1
|
作者
Yuan, Yu [1 ,2 ]
Tao, Yezheng [2 ]
Deng, Yongzhi [3 ,4 ]
Ye, Qunhui [1 ]
Lin, Bin [1 ]
Wu, Lin [1 ,2 ]
机构
[1] Wenzhou Med Univ, Dept Cardiol, Affiliated Wenling Hosp, Wenling 317500, Zhejiang, Peoples R China
[2] Xinxiang Med Univ, Affiliated Hosp Xinxiang 1, Dept Cardiol, Xinxiang 453100, Henan, Peoples R China
[3] Shanxi Med Univ, Affiliated Cardiovasc Hosp, Taiyuan 030024, Shanxi, Peoples R China
[4] Shanxi Cardiovasc Hosp Inst, Dept Cardiovasc Surg, Taiyuan 030024, Shanxi, Peoples R China
关键词
BMP4; myocardial hypertrophy; ERK1/2 signaling pathway; BONE MORPHOGENETIC PROTEIN-4; ANTAGONISTS; APOPTOSIS; ATRIAL;
D O I
10.1590/1678-4324-2019180699
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
Bone morphogenetic protein-4 (BMP4) is a member of the bone morphogenetic protein family which plays an important role in bone formation, inflammation and cardiac hypertrophy. The aim of this study was to investigate the underlying molecular mechanism that BMP4-induced cardiomyocyte hypertrophy. H9c2 cells were used to measure cell surface area and protein synthesis. Western blot was used to examine hypertrophic marker brain natriuretic peptide (BNP) protein expression and phosphorylation of ERK1/2. The results exhibited that cell surface area, protein synthesis and BNP protein expression were increased with BMP4 treatment. While PD98059 inhibited these effects of BMP4. In addition, BMP4 treatment increased phosphorylation of ERK1/2 in a time- and dose-dependent manner. PD98059 treatment decreased phosphorylation of ERK1/2 that was increased by BMP4. These results suggest that BMP4 induces cardiomyocyte hypertrophy through the activation of ERK1/2 cell signaling pathway.
引用
收藏
页码:1 / 11
页数:11
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