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.
Article
in English
| 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.
Full text:
Available
Index:
WPRIM (Western Pacific)
Main subject:
Pharmacology
/
Transcription, Genetic
/
RNA, Messenger
/
Cytokines
/
Atrial Natriuretic Factor
/
Rats, Sprague-Dawley
/
Cardiomegaly
/
Mitogen-Activated Protein Kinase 1
/
MAP Kinase Signaling System
/
Cell Biology
Limits:
Animals
Language:
English
Journal:
Asian Pacific Journal of Tropical Medicine
Year:
2014
Type:
Article
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