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Titolo:
The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy
Autore:
Liao, P; Georgakopoulos, D; Kovacs, A; Zheng, MZ; Lerner, D; Pu, HY; Saffitz, J; Chien, K; Xiao, RP; Kass, DA; Wang, YB;
Indirizzi:
Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 ept Physiol, Baltimore, MD 21201 USA Johns Hopkins Med Inst, Dept Med, Div Cardiol, Baltimore, MD 21205 USA Johns Hopkins Med Inst Baltimore MD USA 21205 ol, Baltimore, MD 21205 USA Washington Univ, Sch Med, Dept Med, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 d, Dept Med, St Louis, MO 63110 USA Washington Univ, Sch Med, Dept Pathol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Pathol, St Louis, MO 63110 USA Univ Calif San Diego, Salk Program Mol Med, Dept Med, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 pt Med, La Jolla, CA 92093 USA Univ Calif San Diego, Salk Program Mol Med, Ctr Genet Mol, La Jolla, CA 92093 USA Univ Calif San Diego La Jolla CA USA 92093 et Mol, La Jolla, CA 92093 USA NIA, Cardiovasc Sci Lab, NIH, Baltimore, MD 21224 USA NIA Baltimore MD USA 21224 rdiovasc Sci Lab, NIH, Baltimore, MD 21224 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 21, volume: 98, anno: 2001,
pagine: 12283 - 12288
SICI:
0027-8424(20011009)98:21<12283:TIVROP>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; N-TERMINAL KINASES; HEART-FAILURE; TRANSGENIC MICE; SELECTIVE ACTIVATION; CONTRACTILE FAILURE; SIGNALING PATHWAY; HYPERTROPHY; EXPRESSION; STRESS;
Keywords:
heart failure; conditional transgenesis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
38
Recensione:
Indirizzi per estratti:
Indirizzo: Wang, YB Univ Maryland, Sch Med, Dept Physiol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 ol, Baltimore, MD 21201 USA
Citazione:
P. Liao et al., "The in vivo role of p38 MAP kinases in cardiac remodeling and restrictive cardiomyopathy", P NAS US, 98(21), 2001, pp. 12283-12288

Abstract

Stress-induced mitogen-activated protein kinase (MAP) p38 is activated in various forms of heart failure, yet its effects on the intact heart remain to be established. Targeted activation of p38 MAP kinase in ventricular myocytes was achieved in vivo by using a gene-switch transgenic strategy with activated mutants of upstream kinases MKK3bE and MKK6bE. Transgene expression resulted in significant induction of p38 kinase activity and premature death at 7-9 weeks. Both groups of transgenic hearts exhibited marked interstitial fibrosis and expression of fetal marker genes characteristic of cardiac failure, but no significant hypertrophy at the organ level. Echocardiographic and pressure-volume analyses revealed a similar extent of systolic contractile depression and restrictive diastolic abnormalities related to markedly increased passive chamber stiffness. However, MKK3bE-expressing hearts had increased end-systolic chamber volumes and a thinned ventricular wall, associated with heterogeneous myocyte atrophy, whereas MKK6bE hearts hadreduced end-diastolic ventricular cavity size, a modest increase in myocyte size, and no significant myocyte atrophy. These data provide in vivo evidence for a negative inotropic and restrictive diastolic e ect from p38 MAP kinase activation in ventricular myocytes and reveal specific roles of p38 pathway in the development of ventricular end-systolic remodeling.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 04/12/20 alle ore 16:44:19