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Titolo:
Rapid tau protein dephosphorylation and differential rephosphorylation during cardiac arrest-induced cerebral ischemia and reperfusion
Autore:
Mailliot, C; Podevin-Dimster, V; Rosenthal, RE; Sergeant, N; Delacourte, A; Fiskum, T; Buee, L;
Indirizzi:
INSERM, U422, F-59045 Lille, France INSERM Lille France F-59045INSERM, U422, F-59045 Lille, France George Washington Univ, Dept Emergency Med, Washington, DC USA George Washington Univ Washington DC USA ergency Med, Washington, DC USA Univ Maryland, Sch Med, Dept Anesthesiol, Baltimore, MD 21201 USA Univ Maryland Baltimore MD USA 21201 Anesthesiol, Baltimore, MD 21201 USA
Titolo Testata:
JOURNAL OF CEREBRAL BLOOD FLOW AND METABOLISM
fascicolo: 3, volume: 20, anno: 2000,
pagine: 543 - 549
SICI:
0271-678X(200003)20:3<543:RTPDAD>2.0.ZU;2-X
Fonte:
ISI
Lingua:
ENG
Soggetto:
HELICAL FILAMENT-TAU; MICROTUBULE-ASSOCIATED PROTEINS; ALZHEIMERS-DISEASE; CYTOSKELETAL PROTEOLYSIS; HUMAN-BRAIN; PHOSPHORYLATION; BINDING; SER(262); KINASE; RESUSCITATION;
Keywords:
Alzheimer's disease; animal model; brain ischemia; microtubule-associated tau proteins; phosphorylation;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
41
Recensione:
Indirizzi per estratti:
Indirizzo: Buee, L INSERM, U422, Pl Verdun, F-59045 Lille, France INSERM Pl Verdun Lille France F-59045 rdun, F-59045 Lille, France
Citazione:
C. Mailliot et al., "Rapid tau protein dephosphorylation and differential rephosphorylation during cardiac arrest-induced cerebral ischemia and reperfusion", J CEREBR B, 20(3), 2000, pp. 543-549

Abstract

The effects of cerebral ischemia/reperfusion on phosphorylation of microtubule-associated tau proteins were assessed in a canine model of cardiac arrest. As tau proteins are phosphorylated by kinases involved in different transduction signal pathways, their phosphorylation state is an excellent marker of neuronal homeostasis and microtubule dynamics. Canine brain tau proteins were characterized by immunoblotting using phosphorylation-dependent antibodies and antisera raised against different amino- and carboxy-terminaltau sequences. The present study reports a complete dephosphorylation of tau proteins during ischemia, which is shown by a higher electrophoretic mobility and the almost (if not total) disappearance of phosphorylation-dependent monoclonal antibody labeling. After 2-hour restoration of spontaneous circulation, a decrease in the electrophoretic mobility was observed, and after 24 hours of reperfusion, a full restoration of the phosphorylation was visualized using phosphorylation-dependent monoclonal antibodies directed against Ser/Thr-Pro sites. However, one particular phosphorylation site involved in tau binding to microtubules, located on Ser(262/356), was never fully significantly rephosphorylated, suggesting that microtubule metabolism was still affected after 24 hours of reperfusion. Thus, the sequential and differential recovery of tau phosphorylation after ischemia followed by reperfusion is a useful marker with which to monitor neuronal integrity after brain ischemia.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 21/09/20 alle ore 19:16:57