中文摘要：

Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated 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^-8and 10^-7mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.

英文摘要：

Objective:To understand the role of ANP mRNA transcription regulation in gpl30-mediated cardiomyocyte hypertrophy,and the involved mitogen-aetivated 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(10-9,10-8and 10-7mol/L).MTT was used to analyze the viability and RT-PCR was used to detect ANP mRNA levels in eardiomyocyte.To inhibit p42/p44 MAPK activity in hypertrophic cardiomyoeytes,the cells were pretreated with a specific MEKI inhibitor.Results:CT-1significantly induced ANP mRNA expression and the viability of canliomyocytes in a doseand time-dependent manner.Furthermore,blocking p42/p44 MAPK activity by the special MEk1 inhibitor uprcgulatcd the ANP mKNA.Conclusions:p42/p44 MAPK have an important role in suppressing ANP mRNA transcription and cell activity in gpl30-mediated hypertrophic ventricular myocytes.