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Titolo:
Activation of cardiac c-Jun NH2-terminal kinases and p38-mitogen-activatedprotein kinases with abrupt changes in hemodynamic load
Autore:
Fischer, TA; Ludwig, S; Flory, E; Gambaryan, S; Singh, K; Finn, P; Pfeffer, MA; Kelly, RA; Pfeffer, JM;
Indirizzi:
Brigham & Womens Hosp, Div Cardiovasc, Boston, MA 02115 USA Brigham & Womens Hosp Boston MA USA 02115 ardiovasc, Boston, MA 02115 USA Harvard Univ, Sch Med, Boston, MA USA Harvard Univ Boston MA USAHarvard Univ, Sch Med, Boston, MA USA Univ Mainz, Dept Med 2, D-6500 Mainz, Germany Univ Mainz Mainz Germany D-6500 Mainz, Dept Med 2, D-6500 Mainz, Germany Univ Wurzburg, Med Ctr, Inst Clin Biochem & Pathobiochem, Wurzburg, Germany Univ Wurzburg Wurzburg Germany iochem & Pathobiochem, Wurzburg, Germany Inst Med Strahlenkunde & Zellforsch, Wurzburg, Germany Inst Med Strahlenkunde & Zellforsch Wurzburg Germany Wurzburg, Germany
Titolo Testata:
HYPERTENSION
fascicolo: 5, volume: 37, anno: 2001,
pagine: 1222 - 1228
SICI:
0194-911X(200105)37:5<1222:AOCCNK>2.0.ZU;2-C
Fonte:
ISI
Lingua:
ENG
Soggetto:
N-TERMINAL KINASES; RAT VENTRICULAR MYOCYTES; SIGNALING PATHWAYS; IN-VITRO; STRESS; HYPERTROPHY; APOPTOSIS; MECHANISMS; MYOCARDIUM; INDUCTION;
Keywords:
hypertrophy; protein kinases; transcription, genetic; hemodynamics;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Clinical Medicine
Life Sciences
Citazioni:
29
Recensione:
Indirizzi per estratti:
Indirizzo: Kelly, RA Brigham & Womens Hosp, Div Cardiovasc, 75 Francis St, Boston, MA02115 USA Brigham & Womens Hosp 75 Francis St Boston MA USA 02115 2115 USA
Citazione:
T.A. Fischer et al., "Activation of cardiac c-Jun NH2-terminal kinases and p38-mitogen-activatedprotein kinases with abrupt changes in hemodynamic load", HYPERTENSIO, 37(5), 2001, pp. 1222-1228

Abstract

The role of mitogen-activated protein kinase (MAPK) pathways as signal transduction intermediates of hemodynamic stress leading to cardiac hypertrophy in the adult heart is not fully established. In a rat model of pressure-overload hypertrophy, we examined whether activation of MAPK pathways, namely, the extracellular signal-regulated protein kinase (ERK), c-Jun NH2-terminal kinase (JNK), and the p38-MAPK pathways, occurs during rapid changes inhemodynamic load in vivo. A slight activation of ERK2 and marked increasesin JNK1 and p38-MAPK activities were observed 30 minutes after aortic banding. The increase in p38-MAPK activity was accompanied by an increase in the phosphorylation of the p38 substrate MAPK-activated protein kinases 2 and3. Activation of these kinases was coincident with an increase in phosphorylation of c-Jun and activating transcription factor-2 (ATF-2) and enhancedDNA binding of activator protein-1 factors. Thus, hemodynamic stress of the adult rat heart in vivo results in rapid activation of several parallel MAPK kinase cascades, particularly stress-activated MAPK and p38-MAPK and their target transcription factors c-Jun and ATF-2.

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Documento generato il 22/09/20 alle ore 20:16:52