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Titolo:
Okadaic acid-induced upregulation of nitrotyrosine and heme oxygenase-1 inrat cortical neuron cultures
Autore:
Kim, DH; Koh, WK; Kim, JU; Lee, JH; Hong, HN;
Indirizzi:
Univ Ulsan, Coll Med, Dept Anat & Cell Biol, Seoul 138736, South Korea Univ Ulsan Seoul South Korea 138736 Cell Biol, Seoul 138736, South Korea Univ Ulsan, Coll Med, Dept Anesthesiol, Seoul 138736, South Korea Univ Ulsan Seoul South Korea 138736 esthesiol, Seoul 138736, South Korea Chonnam Natl Univ, Coll Vet Med, Dept Anat, Kwangju, South Korea Chonnam Natl Univ Kwangju South Korea , Dept Anat, Kwangju, South Korea
Titolo Testata:
NEUROSCIENCE LETTERS
fascicolo: 1, volume: 297, anno: 2001,
pagine: 33 - 36
SICI:
0304-3940(20010105)297:1<33:OAUONA>2.0.ZU;2-N
Fonte:
ISI
Lingua:
ENG
Soggetto:
ALZHEIMERS-DISEASE; OXIDATIVE DAMAGE; TAU; BRAIN; DNA;
Keywords:
okadaic acid; neuronal cells; oxidative damage; Alzheimer's disease;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
20
Recensione:
Indirizzi per estratti:
Indirizzo: Kim, DH Univ Ulsan, Coll Med, Dept Anat & Cell Biol, 388-1 PoongNap-Dong, Seoul 138736, South Korea Univ Ulsan 388-1 PoongNap-Dong Seoul South Korea138736 uth Korea
Citazione:
D.H. Kim et al., "Okadaic acid-induced upregulation of nitrotyrosine and heme oxygenase-1 inrat cortical neuron cultures", NEUROSCI L, 297(1), 2001, pp. 33-36

Abstract

Hyperphosphorylation of tau is a characteristic feature of the neurodegenerative pathology in Alzheimer's disease (AD). Okadaic acid (OA) is currently used in models of AD research to increase the phosphorylation of tau. Using immunocytochemistry and fluorescent study, we found that markers of oxidative activity such as nitrotyrosine, c-jun, 2',7'-dichlorofluorescein diacetate (DCF), and heme oxygenase-1 (HO-1) were altered in OA-treated culture. Immunoreactivity of nitrotyrosine and c-jun, and DCF-oxidation were increased in degenerating neurons, while HO-1 expression was increased in astrocyte in response to OA. The data suggest that tau phosphorylation and oxidative damage be implicated in OA-induced neurodegeneration. (C) 2001 ElsevierScience Ireland Ltd. 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 20:30:41