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Titolo:
Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury
Autore:
Okonkwo, DO; Buki, A; Siman, R; Povlishock, JT;
Indirizzi:
Virginia8Commonwealth Univ, Med Coll Virginia, Dept Anat, Richmond, VA 2329 Virginia Commonwealth Univ Richmond VA USA 23298 Anat, Richmond, VA 2329 Univ Pecs, Sch Med, Dept Neurosurg, H-7624 Pecs, Hungary Univ Pecs Pecs Hungary H-7624 Med, Dept Neurosurg, H-7624 Pecs, Hungary Cephalon, W Chester, PA 19380 USA Cephalon W Chester PA USA 19380Cephalon, W Chester, PA 19380 USA
Titolo Testata:
NEUROREPORT
fascicolo: 2, volume: 10, anno: 1999,
pagine: 353 - 358
SICI:
0959-4965(19990205)10:2<353:CALCAD>2.0.ZU;2-#
Fonte:
ISI
Lingua:
ENG
Soggetto:
AXOLEMMAL PERMEABILITY; MECHANISMS; RAT; MITOCHONDRIA; ISCHEMIA;
Keywords:
axonal injury; calpain; cyclosporin A; mitochondrial permeability transition; PT pore; trauma;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Povlishock, JT Virginiamond,onwealth Univ, Med Coll Virginia, Dept Anat, Box 980-709, Rich Virginia Commonwealth Univ Box 980-709 Richmond VA USA 23298
Citazione:
D.O. Okonkwo et al., "Cyclosporin A limits calcium-induced axonal damage following traumatic brain injury", NEUROREPORT, 10(2), 1999, pp. 353-358

Abstract

IN traumatic axonal injury, Ca2+ influx across a focally damaged axolemma precipitates local mitochondrial failure, degradation of the subaxolemmal spectrin network and compaction of neurofilaments, which collectively contribute to axonal failure. In previous studies, cyclosporin A pretreatment preserved mitochondrial integrity and attenuated axonal failure following trauma. Here we investigate whether this CsA-linked protection was related to the concomitant blunting of intra-axonal, Ca2+-induced cytoskeletal changes in traumatic axonal injury, assessed with antibodies targeting spectrin proteolysis and neurofilament compaction. CsA pretreatment dramatically reduced Ca2+-induced cytoskeletal damage following injury; CsA-treated rats, compared with vehicle-treated rats, displayed a 70% decrease in immunoreactive/damaged profiles. We suggest that CsA-mediated preservation of mitochondrial integrity enables the restoration of ionic and metabolic homeostasis thereby short-circuiting Ca2+-induced proteolysis in injured axons. (C) 1999 Lippincott Williams & Wilkins.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 31/03/20 alle ore 10:22:09