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Titolo:
Oxidative stress induces proorphanin FQ and proenkephalin gene expression in astrocytes through p38-and ERK-MAP kinases and NF-kappa B
Autore:
Rosenberger, J; Petrovics, G; Buzas, B;
Indirizzi:
Uniformed Serv Univ Hlth Sci, Dept Pharmacol, Bethesda, MD 20814 USA Uniformed Serv Univ Hlth Sci Bethesda MD USA 20814 Bethesda, MD 20814 USA
Titolo Testata:
JOURNAL OF NEUROCHEMISTRY
fascicolo: 1, volume: 79, anno: 2001,
pagine: 35 - 44
SICI:
0022-3042(200110)79:1<35:OSIPFA>2.0.ZU;2-V
Fonte:
ISI
Lingua:
ENG
Soggetto:
ACTIVATED PROTEIN-KINASE; PREPROENKEPHALIN MESSENGER-RNA; SIGNAL-REGULATED KINASE; BRAIN INJURY; ORPHANIN-FQ; NOCICEPTIN/ORPHANIN FQ; TRANSCRIPTION FACTOR; CULTURED ASTROCYTES; NEUROPEPTIDE GENE; CYCLIC-AMP;
Keywords:
astrocyte; mitogen-activated protein kinase; nociceptin; nuclear factor-kappa B; orphanin FQ; oxidative stress;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
46
Recensione:
Indirizzi per estratti:
Indirizzo: Buzas, B Uniformed Serv Univ Hlth Sci, Dept Pharmacol, 4301 Jones Bridge Rd, Bethesda, MD 20814 USA Uniformed Serv Univ Hlth Sci 4301 Jones Bridge RdBethesda MD USA 20814
Citazione:
J. Rosenberger et al., "Oxidative stress induces proorphanin FQ and proenkephalin gene expression in astrocytes through p38-and ERK-MAP kinases and NF-kappa B", J NEUROCHEM, 79(1), 2001, pp. 35-44

Abstract

Oxidative stress has been implicated in the pathogenesis of stroke, traumatic brain injuries, and neurodegenerative diseases affecting both neuronal and glial cells in the CNS. In this study we have demonstrated that reactive oxygen species (ROS) dramatically induce the expression of two neuropeptide genes, the opioid proenkephalin (pENK) and the opioid-related proorphanin FQ (pOFQ; also known as pronociceptin) in primary astrocytes. Hydrogen peroxide (H2O2) treatment dose-dependently increased pENK and pOFQ mRNA levels with a maximal effect (similar to 15-fold increase) being detected at 50 muM concentration. Exposing the astrocyte cultures to hypoxia and subsequent re-oxygenation also led to a profound elevation of pOFQ and pENK mRNA levels. Western blot analysis and immunocytochemistry revealed that H2O2 treatment elicited the phosphorylation and nuclear translocation of ERK 1/2 and p38 MAP kinases. Blockade of the p38 or the ERK MAP kinase pathways (by SB202190 and PD98059, respectively) prevented the H2O2-induced increase in pENK and pOFQ mRNA levels indicating a central role for these cascades in the regulation of pOFQ and pENK genes In response to oxidative stress. Regulation of pOFQ and pENK gene expression by ERK and p38 activation may be mediated through the transcription factor cAMP-response element binding protein (CREB). We observed CREB phosphorylation in response to H2O2, which was alsoprevented by SB202190 and PD98059. The nuclear factor-kappaB (NF-kappaB) pathway appears to be involved exclusively in the induction of pOFQ transcription by H2O2, as NF-kappaB inhibitors antagonized the effect of oxidative stress on pOFQ, but not on pENK expression. The profound induction of thesegenes by oxidative stress and these other factors may suggest a role for orphanin FQ and enkephalin in injury and stress responses of the CNS and neuropathophysiological conditions involving reactive oxygen species.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 05/04/20 alle ore 03:58:29