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

AUTOR(ES)

Yuan, Yu

FONTE

Braz. arch. biol. technol.

DATA DE PUBLICAÇÃO

20/12/2019

RESUMO

Abstract 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.

Documentos Relacionados

• Odanacatib Inhibits Resistin-induced Hypertrophic H9c2 Cardiomyoblast Cells Through LKB1/AMPK Pathway
• The MEK1–ERK1/2 signaling pathway promotes compensated cardiac hypertrophy in transgenic mice
• CIRBP protects H9C2 cells against myocardial ischemia through inhibition of NF-κB pathway
• Phospholipase C δ-4 overexpression upregulates ErbB1/2 expression, Erk signaling pathway, and proliferation in MCF-7 cells
• Protective effect of Rheum turkestanikum root against doxorubicin-induced toxicity in H9c2 cells