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Citations to this article

Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy.
G Choukroun, … , A Rosenzweig, T Force
G Choukroun, … , A Rosenzweig, T Force
Published October 1, 1998
Citation Information: J Clin Invest. 1998;102(7):1311-1320. https://doi.org/10.1172/JCI3512.
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Research Article

Role of the stress-activated protein kinases in endothelin-induced cardiomyocyte hypertrophy.

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Abstract

The signal transduction pathways governing the hypertrophic response of cardiomyocytes are not well defined. Constitutive activation of the stress-activated protein kinase (SAPK) family of mitogen-activated protein (MAP) kinases or another stress-response MAP kinase, p38, by overexpression of activated mutants of various components of the pathways is sufficient to induce a hypertrophic response in cardiomyocytes, but it is not clear what role these pathways play in the response to physiologically relevant hypertrophic stimuli. To determine the role of the SAPKs in the hypertrophic response, we used adenovirus-mediated gene transfer of SAPK/ERK kinase-1 (KR) [SEK-1(KR)], a dominant inhibitory mutant of SEK-1, the immediate upstream activator of the SAPKs, to block signal transmission down the SAPK pathway in response to the potent hypertrophic agent, endothelin-1 (ET-1). SEK-1(KR) completely inhibited ET-1-induced SAPK activation without affecting activation of the other MAP kinases implicated in the hypertrophic response, p38 and extracellular signal-regulated protein kinases (ERK)-1/ERK-2. Expression of SEK-1(KR) markedly inhibited the ET-1-induced increase in protein synthesis. In contrast, the MAPK/ERK kinase inhibitor, PD98059, which blocks ERK activation, and the p38 inhibitor, SB203580, had no effect on ET-1-induced protein synthesis. ET-1 also induced a significant increase in atrial natriuretic factor mRNA expression as well as in the percentage of cells with highly organized sarcomeres, responses which were also blocked by expression of SEK-1(KR). In summary, inhibiting activation of the SAPK pathway abrogated the hypertrophic response to ET-1. These data are the first demonstration that the SAPKs are necessary for the development of agonist-induced cardiomyocyte hypertrophy, and suggest that in response to ET-1, they transduce critical signals governing the hypertrophic response.

Authors

G Choukroun, R Hajjar, J M Kyriakis, J V Bonventre, A Rosenzweig, T Force

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Total citations by year

Year: 2022 2021 2020 2019 2018 2017 2016 2015 2014 2013 2012 2011 2010 2009 2008 2007 2006 2005 2004 2003 2002 2001 2000 1999 1978 Total
Citations: 1 1 3 2 3 1 1 2 2 6 5 2 3 4 6 4 9 8 6 14 11 23 29 7 2 155
Citation information
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Citations to this article in year 2012 (5)

Title and authors Publication Year
JNK modulates FOXO3a for the expression of the mitochondrial death and mitophagy marker BNIP3 in pathological hypertrophy and in heart failure
AH Chaanine, D Jeong, L Liang, ER Chemaly, K Fish, RE Gordon, RJ Hajjar
Cell Death and Disease 2012
The role of the paracrine/autocrine mediator endothelin-1 in regulation of cardiac contractility and growth
FM Drawnel, CR Archer, HL Roderick
British Journal of Pharmacology 2012
Role of Endothelin in the Induction of Cardiac Hypertrophy In Vitro
T Bupha-Intr, KM Haizlip, PM Janssen
PloS one 2012
Characterization of hsp27 kinases activated by elevated aortic pressure in heart
B Boivin, M Khairallah, R Cartier, BG Allen
Molecular and Cellular Biochemistry 2012
Regulation of cardiac melusin gene expression by hypertrophic stimuli in the rat
J Aro, H Tokola, VP Ronkainen, E Koivisto, O Tenhunen, M Ilves, I Szokodi, H Ruskoaho, J Rysä
Acta Physiologica 2012

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