Key result
CT-1 induced ANP mRNA expression and cardiomyocyte viability, while blocking p42/p44 MAPK activity with a MEK1 inhibitor upregulated ANP mRNA in hypertrophic ventricular myocytes.
In isolated neonatal ventricular myocytes, p42/p44 MAPK plays an important role in suppressing ANP mRNA transcription during gp130-mediated hypertrophy.
Should not change clinical practice; hypothesis-generating for MAPK-ANP signaling in gp130-mediated hypertrophy.
OBJECTIVE: To understand the role of ANP mRNA transcription regulation in gp130-mediated cardiomyocyte hypertrophy, and the involved mitogen-activated protein kinase kinase (MEK)-extracellular signal-regulated kinase (ERK, also called p42/p44 MAPK) signaling pathway. METHODS: Isolated neonatal ventricular myocytes were treated with different concentrations of CT-1 (10(-9), 10(-8)and 10(-7)mol/L). MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in cardiomyocyte. To inhibit p42/p44 MAPK activity in hypertrophic cardiomyocytes, the cells were pretreated with a specific MEK1 inhibitor. RESULTS: CT-1 significantly induced ANP mRNA expression and the viability of cardiomyocytes in a dose- and time-dependent manner. Furthermore, blocking p42/p44 MAPK activity by the special MEK1 inhibitor upregulated the ANP mRNA. CONCLUSIONS: p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gp130-mediated hypertrophic ventricular myocytes.
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Zhan-ling et al. (2014) studied gp130-mediated cardiomyocyte hypertrophy. CT-1 and specific MEK1 inhibitor was evaluated on ANP mRNA expression and cell viability. CT-1 induced ANP mRNA expression and cardiomyocyte viability, while blocking p42/p44 MAPK activity with a MEK1 inhibitor upregulated ANP mRNA in hypertrophic ventricular myocytes.
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