p42/p44 mitogen-activated protein kinases inhibit atrial natriuretic peptide mRNA transcription in gp130-mediated hypertrophic ventricular myocytes
Asian Pacific Journal of Tropical Medicine
;
(12): 216-220, 2014.
Artigo
em Inglês
| WPRIM
| ID: wpr-819702
ABSTRACT
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.
Texto completo:
DisponíveL
Índice:
WPRIM (Pacífico Ocidental)
Assunto principal:
Farmacologia
/
Transcrição Gênica
/
RNA Mensageiro
/
Citocinas
/
Fator Natriurético Atrial
/
Ratos Sprague-Dawley
/
Cardiomegalia
/
Proteína Quinase 1 Ativada por Mitógeno
/
Sistema de Sinalização das MAP Quinases
/
Biologia Celular
Limite:
Animais
Idioma:
Inglês
Revista:
Asian Pacific Journal of Tropical Medicine
Ano de publicação:
2014
Tipo de documento:
Artigo
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