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Titolo:
Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury
Autore:
Dore, S; Takahashi, M; Ferris, CD; Hester, LD; Guastella, D; Snyder, SH;
Indirizzi:
Johns Hopkins Univ, Sch Med, Dept Neurosci, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 urosci, Baltimore, MD 21205 USA JohnsUSApkins Univ, Sch Med, Dept Pharmacol & Mol Sci, Baltimore, MD 21205Johns Hopkins Univ Baltimore MD USA 21205 & Mol Sci, Baltimore, MD 21205 Johns Hopkins Univ, Sch Med, Dept Med, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 pt Med, Baltimore, MD 21205 USA Johns Hopkins Univ, Sch Med, Dept Psychiat, Baltimore, MD 21205 USA Johns Hopkins Univ Baltimore MD USA 21205 ychiat, Baltimore, MD 21205 USA
Titolo Testata:
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
fascicolo: 5, volume: 96, anno: 1999,
pagine: 2445 - 2450
SICI:
0027-8424(19990302)96:5<2445:BFBAOH>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
GLUTATHIONE-S-TRANSFERASES; HIPPOCAMPAL-NEURONS; CARBON-MONOXIDE; RAT-BRAIN; KINASE-C; ALBUMIN; ANTIOXIDANT; PLASMA; PREVENTION; EXPRESSION;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
53
Recensione:
Indirizzi per estratti:
Indirizzo: Snyder, SH Johns1205kins Univ, Sch Med, Dept Neurosci, 725 N Wolfe St, Baltimore, MD 2 Johns Hopkins Univ 725 N Wolfe St Baltimore MD USA 21205 , MD 2
Citazione:
S. Dore et al., "Bilirubin, formed by activation of heme oxygenase-2, protects neurons against oxidative stress injury", P NAS US, 96(5), 1999, pp. 2445-2450

Abstract

Heme oxygenase (HO) catalyzes the conversion of heme to carbon monoxide, iron, and biliverdin, which is immediately reduced to bilirubin (BR), Two HOactive isozymes exist: HO1, an inducible heat shock protein, and HO2, which is constitutive and highly concentrated in neurons. We demonstrate a neuroprotective role for BR formed from HO2. Neurotoxicity elicited by hydrogenperoxide in hippocampal and cortical neuronal cultures is prevented by thephorbol ester, phorbol 12-myristate 13-acetate (PMA) via stimulation of protein kinase C. We observe phosphorylation of HO2 through the protein kinase C pathway with enhancement of HO2 catalytic activity and accumulation of BR in neuronal cultures. The neuroprotective effects of PMA are prevented by the HO inhibitor tin protoporphyrin IX and in cultures from mice with deletion of HO2 gene. Moreover, BR, an antioxidant, is neuroprotective at nanomolar concentrations.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 20/09/20 alle ore 04:41:59