Key result
BMP4 promotes cardiomyocyte hypertrophy via ERK1/2 signaling, which is attenuated by PD98059.
Why the study?
The molecular mechanism by which BMP4 induces cardiomyocyte hypertrophy was not fully understood.
Does BMP4 induce cardiomyocyte hypertrophy through the ERK1/2 signaling pathway in H9c2 cells?
Does BMP4 induce cardiomyocyte hypertrophy through the ERK1/2 signaling pathway in H9c2 cells?
BMP4 induces cardiomyocyte hypertrophy in vitro through the activation of the ERK1/2 signaling pathway.
In vitro data support targeted pathway studies; leaves open translation to in vivo or clinical hypertrophy models.
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.
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Yuan et al. (2019) studied Cardiomyocyte hypertrophy. BMP4 vs. PD98059 / Control was evaluated on Cell surface area, protein synthesis, BNP protein expression, and phosphorylation of ERK1/2. BMP4 induces cardiomyocyte hypertrophy through the activation of the ERK1/2 cell signaling pathway, an effect that is inhibited by PD98059.
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