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Titolo:
Myocardial ischemia activates the JAK-STAT pathway through angiotensin II signaling in in vivo myocardium of rats
Autore:
Omura, T; Yoshiyama, M; Ishikura, F; Kobayashi, H; Takeuchi, K; Beppu, S; Yoshikawa, J;
Indirizzi:
Osaka City Univ, Sch Med, Dept Internal Med 1, Abeno Ku, Osaka 5458585, Japan Osaka City Univ Osaka Japan 5458585 ed 1, Abeno Ku, Osaka 5458585, Japan Osaka City Univ, Fac Med, Sch Allied Hlth Sci, Osaka 558, Japan Osaka CityUniv Osaka Japan 558 d, Sch Allied Hlth Sci, Osaka 558, Japan
Titolo Testata:
JOURNAL OF MOLECULAR AND CELLULAR CARDIOLOGY
fascicolo: 2, volume: 33, anno: 2001,
pagine: 307 - 316
SICI:
0022-2828(200102)33:2<307:MIATJP>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
LEUKEMIA INHIBITORY FACTOR; CONGESTIVE-HEART-FAILURE; RECEPTOR ANTAGONIST; JAK/STAT PATHWAY; CARDIAC MYOCYTES; PROTEIN-KINASES; NITRIC-OXIDE; IN-VIVO; INFARCTION; EXPRESSION;
Keywords:
myocardial infarction; janus kinase (JAK); signal transducer and activator of transcription (STAT); sis-inducing factor (SIF); angiotensin II;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Omura, T Osaka City Univ, Sch Med, Dept Internal Med 1, Abeno Ku, 1-4-3 Asahimachi,Osaka 5458585, Japan Osaka City Univ 1-4-3 Asahimachi Osaka Japan5458585 8585, Japan
Citazione:
T. Omura et al., "Myocardial ischemia activates the JAK-STAT pathway through angiotensin II signaling in in vivo myocardium of rats", J MOL CEL C, 33(2), 2001, pp. 307-316

Abstract

There have been many studies concerning the hemodynamics and physiologicalmechanisms in ischemic heart disease, little is known about molecular mechanisms during myocardial ischemia in in vivo study. As the signal transduction pathway responsible for myocardial hypertrophy and apoptosis, janus kinase (JAK) and signal transducers and activators of transcription (STAT) aresuggested to play an important role. However, whether in vivo activation of JAK-STAT pathway occurs during myocardial ischemia is still unknown. The purpose of this study was to determine whether myocardial JAK or STAT is activated in ischemic heart, and to evaluate the angiotensin blockade on the pathway Myocardial infarction was produced by ligation of the coronary artery in Wistar rats. After myocardial ischemia, we analysed both activated levels and total amounts of JAK1, JAK2, STAT1 and STAT3 by Western blot analyses at 0, 5 15, 30, 60, 120 and 240 min. Compared with JAK activities at 0 min, JAK1 activities were significantly increased at 60 and 120 min (3.0- and 3.7-fold, respectively, P<0.01). JAK2 and STAT1 activities of ischemic myocardium were unchanged through the time course. STAT3 activities were increased at 5 min (3.3-fold, P<0.01) and markedly enhanced at 30, 60 and 120 min (4.6-, 7,7- and 8.7-fold, respectively P<0.01). Pretreatment with imidapril (ACE inhibitor) and candesartan cilexitil (AT1 receptor antagonist) significantly prevented the increase in the phosphorylation of JAK1 at 120 min and STAT3 at 30 and 120 min, Sis-inducing factor (SIF) DNA complex was supershifed by specific anti-STAT3 antibody, indicating that increased SIF complex at least contained activated STAT3 proteins in ischemic myocardium. Imidapril and candesartan cilexitil inhibited the activation of SIF DNA binding at 1 day after coronary ligation, In conclusion, we showed that JAK1 and STAT3 were activated by ischemia from the basal activities in in vivo ratmyocardial ischemia model, Imidapril and candesartan cilexitil prevented the increase in phosphorylated JAK1 and STAT3, thereby suggesting that angiotensin II, especially angiotensin II type I receptor, partially mediates activation of myocardial JAK-STAT pathway in acute myocardial ischemia. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 18:29:51