Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Gene program for cardiac cell survival induced by transient ischemia in conscious pigs
Autore:
Depre, C; Tomlinson, JE; Kudej, RK; Gaussin, V; Thompson, E; Kim, SJ; Vatner, DE; Topper, JN; Vatner, SF;
Indirizzi:
Hackensack Univ, Med Ctr, Inst Cardiovasc Res, Hackensack, NJ 07601 USA Hackensack Univ Hackensack NJ USA 07601 asc Res, Hackensack, NJ 07601 USA Univ Med & Dent New Jersey, New Jersey Med Sch, Dept Med, Inst Cardiovasc Res, Newark, NJ 07103 USA Univ Med & Dent New Jersey Newark NJ USA 07103 Res, Newark, NJ 07103 USA COR Therapeut Inc, S San Francisco, CA 94080 USA COR Therapeut Inc S San Francisco CA USA 94080 an Francisco, CA 94080 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 16, volume: 98, anno: 2001,
pagine: 9336 - 9341
SICI:
0027-8424(20010731)98:16<9336:GPFCCS>2.0.ZU;2-3
Fonte:
ISI
Lingua:
ENG
Soggetto:
PLASMINOGEN-ACTIVATOR INHIBITOR-1; ANKYRIN REPEAT PROTEIN; INDUCED APOPTOSIS; PORCINE MYOCARDIUM; STUNNED MYOCARDIUM; HT1080 CELLS; CYTOCHROME-C; EXPRESSION; GROWTH; TRANSCRIPTION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
47
Recensione:
Indirizzi per estratti:
Indirizzo: Depre, C Hackensack Univ, Med Ctr, Inst Cardiovasc Res, Res Bldg,Room 338,30 Prospect Ave, Hackensack, NJ 07601 USA Hackensack Univ Res Bldg,Room 338,30 Prospect Ave Hackensack NJ USA 07601
Citazione:
C. Depre et al., "Gene program for cardiac cell survival induced by transient ischemia in conscious pigs", P NAS US, 98(16), 2001, pp. 9336-9341

Abstract

Therapy for ischemic heart disease has been directed traditionally at limiting cell necrosis. We determined by genome profiling whether ischemic myocardium can trigger a genetic program promoting cardiac cell survival which would be a novel and potentially equally important mechanism of salvage. Although cardiac genomics is usually performed in rodents, we used a swine model of ischemia/reperfusion followed by ventricular dysfunction (stunning),which more closely resembles clinical conditions. Gene expression profileswere compared by subtractive hybridization between ischemic and normal tissue of the same hearts. About one-third (23/74) of the nuclear-encoded genes that were upregulated in ischemic myocardium participate in survival mechanisms (inhibition of apoptosis, cytoprotection, cell growth, and stimulation of translation). The specificity of this response was confirmed by Northern blot and quantitative PCR. Unexpectedly, this program also included genes not previously described iri cardiomyocytes. Up-regulation of survival genes was more profound in subendocardium over subepicardium, reflecting that this response in stunned myocardium was proportional to the severity of the ischemic insult. Thus, in a swine model that recapitulates human heart disease, nonlethal ischemia activates a genomic program of cell survival that relates to the time course of myocardial stunning and differs transmurally in relation to ischemic stress, which induced the stunning. Understandingthe genes up-regulated during myocardial stunning, including those not previously described in the heart, and developing strategies that activate this program may open new avenues for therapy in ischemic heart disease.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 28/09/20 alle ore 15:13:58