Titre
Angiotensin II-induced cardiac hypertrophy is associated with different mitogen-activated protein kinase activation in normotensive and hypertensive mice.
Type
article
Institution
UNIL/CHUV/Unisanté + institutions partenaires
Périodique
Auteur(s)
Pellieux, C.
Auteure/Auteur
Sauthier, T.
Auteure/Auteur
Aubert, J.F.
Auteure/Auteur
Brunner, H.R.
Auteure/Auteur
Pedrazzini, T.
Auteure/Auteur
Liens vers les personnes
Liens vers les unités
ISSN
0263-6352
Statut éditorial
Publié
Date de publication
2000
Volume
18
Numéro
9
Première page
1307
Dernière page/numéro d’article
17
Peer-reviewed
Oui
Langue
anglais
Notes
Publication types: In Vitro ; Journal Article ; Research Support, Non-U.S. Gov't - Publication Status: ppublish
Résumé
OBJECTIVE: In addition to its haemodynamic effects, angiotensin II (AngII) is thought to contribute to the development of cardiac hypertrophy via its growth factor properties. The activation of mitogen-activated protein kinases (MAPK) is crucial for stimulating cardiac growth. Therefore, the present study aimed to determine whether the trophic effects of AngII and the AngII-induced haemodynamic load were associated with specific cardiac MAPK pathways during the development of hypertrophy. Methods The activation of the extracellular-signal-regulated kinase (ERK), the c-jun N-terminal kinase (JNK) and the p38 kinase was followed in the heart of normotensive and hypertensive transgenic mice with AngII-mediated cardiac hypertrophy. Secondly, we used physiological models of AngII-dependent and AngII-independent renovascular hypertension to study the activation of cardiac MAPK pathways during the development of hypertrophy. RESULTS: In normotensive transgenic animals with AngII-induced cardiac hypertrophy, p38 activation is associated with the development of hypertrophy while ERK and JNK are modestly stimulated. In hypertensive transgenic mice, further activation of ERK and JNK is observed. Moreover, in the AngII-independent model of renovascular hypertension and cardiac hypertrophy, p38 is not activated while ERK and JNK are strongly stimulated. In contrast, in the AngII-dependent model, all three kinases are stimulated. CONCLUSIONS: These data suggest that p38 activation is preferentially associated with the direct effects of AngII on cardiac cells, whereas stimulation of ERK and JNK occurs in association with AngII-induced mechanical stress.
Sujets
PID Serval
serval:BIB_71CCF0DF10B0
PMID
Date de création
2008-01-25T07:45:29.375Z
Date de création dans IRIS
2025-05-20T23:57:17Z