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Titolo:
Temporospatial expression of HSP72 and c-JUN, and DNA fragmentation in goat hippocampus after global cerebral ischemia
Autore:
Torregrosa, G; Barbera, MD; Orti, M; Centeno, JM; Salom, JB; Justicia, C; Planas, AM; Alborch, E;
Indirizzi:
Hosp Univ La Fe, Ctr Invest, Valencia 46009, Spain Hosp Univ La Fe Valencia Spain 46009 , Ctr Invest, Valencia 46009, Spain Univ Valencia, Fac Ciencies Biol, Unitat Fisiol, Dept Biol Anim, Valencia,Spain Univ Valencia Valencia Spain tat Fisiol, Dept Biol Anim, Valencia,Spain Univ Valencia, Fac Med, Dept Fisiol, Valencia, Spain Univ Valencia Valencia Spain cia, Fac Med, Dept Fisiol, Valencia, Spain CSIC, Inst Invest Biomed Barcelona, Dept Farmacol & Toxicol, Barcelona, Spain CSIC Barcelona Spain rcelona, Dept Farmacol & Toxicol, Barcelona, Spain
Titolo Testata:
HIPPOCAMPUS
fascicolo: 2, volume: 11, anno: 2001,
pagine: 146 - 156
SICI:
1050-9631(2001)11:2<146:TEOHAC>2.0.ZU;2-G
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; HEAT-SHOCK-PROTEIN; SELECTIVE NEURONAL VULNERABILITY; EARLY GENE-EXPRESSION; GERBIL HIPPOCAMPUS; MESSENGER-RNA; RAT-BRAIN; TEMPORAL PROFILE; IONIZING-RADIATION; IN-SITU;
Keywords:
delayed neuronal death; heat shock proteins; immediate early genes; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
48
Recensione:
Indirizzi per estratti:
Indirizzo: Torregrosa, G Hosp Univ La Fe, Ctr Invest, Ave Campanar 21, Valencia 46009, Spain Hosp Univ La Fe Ave Campanar 21 Valencia Spain 46009 Spain
Citazione:
G. Torregrosa et al., "Temporospatial expression of HSP72 and c-JUN, and DNA fragmentation in goat hippocampus after global cerebral ischemia", HIPPOCAMPUS, 11(2), 2001, pp. 146-156

Abstract

The role of gene induction (expression of HSP72 and c-JUN proteins) and delayed ischemic cell death (in situ labeling of DNA fragmentation) have beeninvestigated in the goat hippocampus after transient global cerebral ischemia. The animals were subjected to 20-min ischemia (bilateral occlusion of the external carotid arteries plus bilateral jugular vein compression) and allowed to reperfuse for 2 h, and then 1, 3, and 7 days. Histological signsof cell loss were not found in the hippocampus at 2 h, 1 day, or 3 days ofreperfusion. However, such an ischemic insult produced extensive, selective, and delayed degeneration in the hippocampus, as 68% of the neurons in CA1 had died at 7 days, but cell loss was not detected in CA3 and dentate gyrus fields. Concomitantly, a high percentage of TUNEL-positive CA1 neurons (60 +/- 9%, mean +/- SEM) was seen at 7 days, but not at the earlier time points. Mild induction of HSP72 was detected in the goat hippocampus after ischemia. The maximum percentage of HSP72-positive neurons (10-15%) was shownat 3 days of reperfusion and was concentrated mainly in the CA3 field, subiculum, and hilus, rather than in the CA1 field, whereas HSP72 expression was hardly detected at 7 days. At this later time point, scattered inductionof nuclear c-JUN was found in a few neurons. The results show that: 1) postischemic delayed neuronal death selectively affects the CA1 field in the goat hippocampus, a phenomenon which seems to take longer to develop than inpreviously reported rodent models; and 2) postischemic expression of c-JUNdoes not appear to be related to cell death or survival, while the inability of most CA1 neurons to express HSP72 could contribute to neuronal death. Hippocampus 2001;11:146-156. (C) 2001 Wiley-Liss, Inc.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 19/09/20 alle ore 23:08:59