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Titolo:
Pericardial fluid from patients with ischemic heart disease induces myocardial cell apoptotis via an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway
Autore:
Iwakura, A; Fujita, M; Hasegawa, K; Toyokuni, S; Sawamura, T; Nohara, R; Sasayama, S; Komeda, M;
Indirizzi:
Kyoto Univ, Coll Med Technol, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ Kyoto Japan 6068507 d Technol, Sakyo Ku, Kyoto 6068507, Japan Kyoto Univ, Grad Sch Med, Dept Cardiovasc Surg, Kyoto, Japan Kyoto Univ Kyoto Japan Grad Sch Med, Dept Cardiovasc Surg, Kyoto, Japan Kyoto Univ, Grad Sch Med, Dept Cardiovasc Med, Kyoto, Japan Kyoto Univ Kyoto Japan Grad Sch Med, Dept Cardiovasc Med, Kyoto, Japan Natl Cardiovasc Res Ctr, Osaka, Japan Natl Cardiovasc Res Ctr Osaka Japan tl Cardiovasc Res Ctr, Osaka, Japan Kyoto Univ, Grad Sch Med, Dept Pathol & Biol Dis, Kyoto, Japan Kyoto UnivKyoto Japan ad Sch Med, Dept Pathol & Biol Dis, Kyoto, Japan
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 3, volume: 33, anno: 2001,
pagine: 419 - 430
SICI:
0022-2828(200103)33:3<419:PFFPWI>2.0.ZU;2-Y
Fonte:
ISI
Lingua:
ENG
Soggetto:
RAT CARDIAC MYOCYTES; TUMOR-SUPPRESSOR P53; SUBSTRATE-SPECIFICITY; UNSTABLE ANGINA; BAX GENE; DEATH; HYPERTROPHY; EXPRESSION; REGULATOR; MAPKS;
Keywords:
apoptosis; p38 MAPK; cardiac myocyte; oxidant stress; ischemic heart disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
42
Recensione:
Indirizzi per estratti:
Indirizzo: Fujita, M Kyoto Univ, Coll Med Technol, Sakyo Ku, 53 Kawahara Cho Shogoin,Kyoto 6068507, Japan Kyoto Univ 53 Kawahara Cho Shogoin Kyoto Japan 6068507 7, Japan
Citazione:
A. Iwakura et al., "Pericardial fluid from patients with ischemic heart disease induces myocardial cell apoptotis via an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway", J MOL CEL C, 33(3), 2001, pp. 419-430

Abstract

Factors produced by the heart are accumulated at high concentrations in pericardial fluid. We recently reported that pericardial fluid from patients with ischemia heart disease induces apoptosis in an F2 cell line. To characterize factors in pericardial fluid from patients with ischemic heart disease, we investigated signaling pathways by which this pericardial fluid induces apoptosis in cardiac myocytes. Pericardial fluid from patients with ischemic heart disease markedly increased the percentage of TUNEL-positive myocytes compared with Fetal bovine serum. Apoptosis was also confirmed by ladder formation and morphologic features. Apoptosis mediated by this pericardial fluid occurs as readily in cardiac myocytes prepared from neonatal micenullizygous for p5.3 as in wild-type littermates. This indicates that p53 is not required for this process. We have found that pericardial fluid fromischemic heart disease elicits a robust increase in phosphorylation of p38mitogen-activated protein kinase. Specific inhibition of tho p38 mitogen-activated protein kinase pathway with SE 203580 almost completely blocked apoptosis mediated by pericardial fluid from ischemic heart disease. Activation of p38 mitogen-activated protein kinase is caused by cellular stress, including oxidants. We have also found that anti-oxidant catalase inhibited pericardial fluid-induced activation of p38 mitogen-activated protein kinaseand apoptosis. These findings demonstrate that myocardial cell apoptosis induced by pericardial fluid from patients with ischemic heart disease is mediated by an oxidant stress-sensitive p38 mitogen-activated protein kinase pathway. A possible application of SE 203580 to preserve cardiac function in patients with ischemic heart disease should be discussed. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 10:17:51