Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
DNA damage and DNA damage-inducible protein Gadd45 following ischemia in the P7 neonatal rat
Autore:
Charriaut-Marlangue, C; Richard, E; Ben-Ari, Y;
Indirizzi:
Univ Paris 05, INSERM, U29, F-75014 Paris, France Univ Paris 05 Paris France F-75014 5, INSERM, U29, F-75014 Paris, France
Titolo Testata:
DEVELOPMENTAL BRAIN RESEARCH
fascicolo: 2, volume: 116, anno: 1999,
pagine: 133 - 140
SICI:
0165-3806(19990906)116:2<133:DDADDP>2.0.ZU;2-H
Fonte:
ISI
Lingua:
ENG
Soggetto:
CEREBRAL HYPOXIA-ISCHEMIA; FOCAL ISCHEMIA; BRAIN-DAMAGE; FOREBRAIN ISCHEMIA; MESSENGER-RNA; GENE GADD45; CELL-DEATH; APOPTOSIS; FRAGMENTATION; EXPRESSION;
Keywords:
neonatal ischemia; DNA damage; Gadd45; DNA repair; apoptosis;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
39
Recensione:
Indirizzi per estratti:
Indirizzo: Charriaut-Marlangue, C Fac Pharm, Pharmacol Lab, 4 Ave Observ, F-75006 Paris, France Fac Pharm 4 Ave Observ Paris France F-75006 France
Citazione:
C. Charriaut-Marlangue et al., "DNA damage and DNA damage-inducible protein Gadd45 following ischemia in the P7 neonatal rat", DEV BRAIN R, 116(2), 1999, pp. 133-140

Abstract

Cerebral ischemia in adult rodents leads to the production of several types of lesions in the genomic DNA, followed by the activation of the damage-response indicator Gadd45. Our purpose was to investigate the structural changes that occur in chromatin DNA and repair processes after ischemic injuryin neonatal brain. Neonatal ischemia was induced by the permanent left MCAocclusion in association with 1 h occlusion of the left common carotid artery in 7-day-old Wistar pups. Oligonucleosome fragments that are recognizedas the characteristic DNA ladder was observed in a delayed fashion. Double-strand breaks result in high molecular weight fragments of 50- and 300-kbpas demonstrated by pulsed-field gel electrophoresis, and visualized by theTUNEL assay at 24 h of recovery. In contrast, DNA single-strand breaks, shown by the use of DNA polymerase I-mediated biotin-dATP nick translation were not so abundant. Gadd45 immunoreactivity was sequentially increased in vulnerable neurons in the infarct (4 to 24 h) and in sublethally injured neurons in the penumbra (24-48 h). Taken together, these findings suggest thatGadd45 responds to DNA damage following neonatal ischemia. Furthermore, repairing processes seem to be more active in the penumbra and therefore Gadd45 could have also a protective role in cerebral ischemia. (C) 1999 Elsevier Science B.V. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 03/04/20 alle ore 20:28:04