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Titolo:
The mitochondrial permeability transition pore and nitric oxide synthase mediate early mitochondrial depolarization in astrocytes during oxygen-glucose deprivation
Autore:
Reichert, SA; Kim-Han, JS; Dugan, LL;
Indirizzi:
Washington Univ, Sch Med, Dept Neurol, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Dept Neurol, St Louis, MO 63110 USA Washington Univ, Sch Med, Ctr Study Nervous Syst Injury, St Louis, MO 63110 USA Washington Univ St Louis MO USA 63110 Syst Injury, St Louis, MO 63110 USA
Titolo Testata:
JOURNAL OF NEUROSCIENCE
fascicolo: 17, volume: 21, anno: 2001,
pagine: 6608 - 6616
SICI:
0270-6474(20010901)21:17<6608:TMPTPA>2.0.ZU;2-F
Fonte:
ISI
Lingua:
ENG
Soggetto:
TRANSIENT FOREBRAIN ISCHEMIA; CYTOCHROME-C RELEASE; CEREBRAL-ISCHEMIA; CORTICAL-NEURONS; GLIAL-CELLS; RAT; GLUTAMATE; APOPTOSIS; BRAIN; NEUROTOXICITY;
Keywords:
tetramethylrhodamine ethyl ester; mitochondrial permeability transition pore; nitric oxide synthase; cyclosporin A; confocal microscopy; cortical cell cultures;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
54
Recensione:
Indirizzi per estratti:
Indirizzo: Dugan, LL Washington Univ, Sch Med, Dept Neurol, 660 S Euclid Ave Box 8111, St Louis, MO 63110 USA Washington Univ 660 S Euclid Ave Box 8111 St LouisMO USA 63110
Citazione:
S.A. Reichert et al., "The mitochondrial permeability transition pore and nitric oxide synthase mediate early mitochondrial depolarization in astrocytes during oxygen-glucose deprivation", J NEUROSC, 21(17), 2001, pp. 6608-6616

Abstract

Recent studies suggest that the degree of mitochondrial dysfunction in cerebral ischemia may be an important determinant of the final extent of tissue injury. Although loss of mitochondrial membrane potential (psi (m)), one index of mitochondrial dysfunction, has been documented in neurons exposed to ischemic conditions, it is not yet known whether astrocytes, which are relatively resistant to ischemic injury, experience changes in psi (m) undersimilar conditions. To address this, we exposed cortical astrocytes cultured alone or with neurons to oxygen-glucose deprivation (OGD) and monitored psi (m) using tetramethylrhodamine ethyl ester. Both neurons and astrocytesexhibited profound loss of psi (m) after 45-60 min of OGD. However, although this exposure is lethal to nearly all neurons, it is hours less than that needed to kill astrocytes. Astrocyte psi (m) was rescued during OGD by cyclosporin A, a permeability transition pore blocker, and N-G-nitro-arginine, a nitric oxide synthase inhibitor. Loss of mitochondrial membrane potential in astrocytes was not accompanied by depolarization of the plasma membrane. Recovery of astrocyte psi (m) after reintroduction of O-2 and glucose occurred over a surprisingly long period (>1 hr), suggesting that OGD causedspecific, reversible changes in astrocyte mitochondrial physiology beyond the simple lack of O-2 and glucose. Decreased psi (m) was associated with acyclosporin A-sensitive loss of cytochrome c but not with activation of caspase-3 or caspase-9. Our data suggest that astrocyte mitochondrial depolarization could be a previously unrecognized event early in ischemia and thatstrategies that target the mitochondrial component of ischemic injury may benefit astrocytes as well as neurons.

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Documento generato il 09/04/20 alle ore 11:01:38