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Titolo:
Differential expression of active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates following quinolinic acid excitotoxicity in the rat
Autore:
Ferrer, I; Blanco, R; Carmona, M;
Indirizzi:
Hosp De Liobregat, Serv Anat Patol, Unitat Neuropatol, Lhospitalet De Llobregat 08907, Spain Hosp De Liobregat Lhospitalet De Llobregat Spain 08907egat 08907, Spain Univ Barcelona, Dept Biol Cellular & Anat Patol, Barcelona, Spain Univ Barcelona Barcelona Spain Cellular & Anat Patol, Barcelona, Spain
Titolo Testata:
MOLECULAR BRAIN RESEARCH
fascicolo: 1-2, volume: 94, anno: 2001,
pagine: 48 - 58
SICI:
0169-328X(20011019)94:1-2<48:DEOAPM>2.0.ZU;2-I
Fonte:
ISI
Lingua:
ENG
Soggetto:
SIGNAL-TRANSDUCTION PATHWAY; EXTRACELLULAR-REGULATED KINASES; TRANSIENT FOREBRAIN ISCHEMIA; N-TERMINAL PHOSPHORYLATION; FOCAL CEREBRAL-ISCHEMIA; JUN NH2-TERMINAL KINASE; PROGRAMMED CELL-DEATH; C-FOS EXPRESSION; PROTEIN-KINASE; PHOSPHATIDYLINOSITOL 3-KINASE;
Keywords:
quinolinic acid; MAPK; ERK; JNK; p38; CREB; ATF-2; Elk-1; c-Jun; c-Myc; caspase-3;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
84
Recensione:
Indirizzi per estratti:
Indirizzo: Ferrer, I Hosp De Liobregat, Serv Anat Patol, Unitat Neuropatol, Feixa Llarga SN, Lhospitalet De Llobregat 08907, Spain Hosp De Liobregat Feixa Llarga SN Lhospitalet De Llobregat Spain 08907
Citazione:
I. Ferrer et al., "Differential expression of active, phosphorylation-dependent MAP kinases, MAPK/ERK, SAPK/JNK and p38, and specific transcription factor substrates following quinolinic acid excitotoxicity in the rat", MOL BRAIN R, 94(1-2), 2001, pp. 48-58

Abstract

Excitotoxicity is considered a major cell death inductor in neurodegeneration. Yet mechanisms involved in cell death and cell survival following excitotoxic insults are poorly understood. Expression of active, phosphorylation-dependent mitogen-activated extracellular signal-regulated kinases (MAPK/ERKs), stress activated c-Jun N-terminal kinases (SAPK/JNKs) and p38 kinases, as well as their putative active specific transcriptional factor substrates CREB, Elk-1, ATF-2, c-Myc and c-Jun, have been examined following intracortical injection of the glutamate analogue quinolinic acid (QA). Increased JNK(P) and p38(P) immunoreactivity has been found in the core at I h following QA injection, whereas increased MAPK(P) immunoreactivity occurs in neurons and glial cells localised around the lesion and in neurons in remote cortical regions. This is accompanied by strong phosphorylated Ser63 c-Jun (c-Jun(P)) immunoreactivity in the core at 3 h, and by strong phosphorylated CREB, Elk-1 and ATF-2 (CREBP, Elk-1(P) and ATF-2(P)) immunoreactivity mainly in neurons around the core at 24 h following QA injection. Examination with the method of in situ end-labelling of nuclear DNA fragmentation has revealed large numbers of positive cells with no apoptotic morphology in thecore at 24 h, thus indicating that JNK(P), p38(P) and c-Jun(P) over-expression precedes cell death. In contrast, MAPK(P), CREBP, Elk-1(P) and ATF-2(P), but not phosphorylated c-Myc (c-Myc(P)), over-expression correlates withcell survival. Examination of cleaved, active caspase-3 has shown specificimmunoreactivity restricted to a few hematogenous cells in the area of injection. Since cleaved caspase-3 is not expressed by dying cells in the present paradigm, JNK(P), p38(P) and c-Jun(P) expression is not associated withcaspase-3 activation. The present results demonstrate selective activationof specific MAPK signals which are involved either in cell death or cell survival triggered by excitotoxic insult. (C) 2001 Elsevier Science BY. All rights reserved.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 13:10:03