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Titolo:
Traumatic brain injury-induced changes in gene expression and functional activity of mitochondrial cytochrome c oxidase
Autore:
Harris, LK; Black, RT; Golden, KM; Reeves, TM; Povlishock, JT; Phillips, LL;
Indirizzi:
Virginia Commonwealth Univ, MCV Stn, Dept Anat, Richmond, VA 23298 USA Virginia Commonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA Virginia Commonwealth Univ, Div Neurosurg, Richmond, VA 23298 USA VirginiaCommonwealth Univ Richmond VA USA 23298 , Richmond, VA 23298 USA
Titolo Testata:
JOURNAL OF NEUROTRAUMA
fascicolo: 10, volume: 18, anno: 2001,
pagine: 993 - 1009
SICI:
0897-7151(200110)18:10<993:TBICIG>2.0.ZU;2-5
Fonte:
ISI
Lingua:
ENG
Soggetto:
MESSENGER-RNA; DIFFERENTIAL DISPLAY; SUPEROXIDE DISMUTASE; TRANSGENIC MICE; RAT HIPPOCAMPUS; DENTATE GYRUS; MODEL; DISEASE; SUBUNIT; DEAFFERENTATION;
Keywords:
cytochrome c oxidase; deafferentation; neuroexcitation; plasticity; traumatic brain injury;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
63
Recensione:
Indirizzi per estratti:
Indirizzo: Harris, LK Virginia Commonwealth Univ, MCV Stn, Dept Anat, 1217 E MarshallSt Rm 7-36,POB 980709, Richmond, VA 23298 USA Virginia Commonwealth Univ 1217 E Marshall St Rm 7-36,POB 980709 Richmond VA USA 23298
Citazione:
L.K. Harris et al., "Traumatic brain injury-induced changes in gene expression and functional activity of mitochondrial cytochrome c oxidase", J NEUROTRAU, 18(10), 2001, pp. 993-1009

Abstract

Traumatic brain injury (TBI) is documented to have detrimental effects on CNS metabolism, including alterations in glucose utilization and the depression of mitochondrial oxidative phosphorylation. Studies on mitochondrial metabolism have also provided evidence for reduced activity of the cytochrome oxidase complex of the electron transport chain (complex IV) after TBI and an immediate (1hr) reduction in mitochondrial state 3 respiratory rate, which can persist for up to 14 days postinjury. Using differential display methods to screen for differences in gene expression, we have found that cytochrome c oxidase H (COII), a mitochondrial encoded subunit of complex IV, is upregulated following TBI. Since COH carries a binding site for cytochrome c in the respiratory chain, and since it is required for the passage of chain electrons to molecular oxygen, driving the production of ATP, we hypothesized that metabolic dysfunction resulting from TBI alters COII gene expression directly, perhaps influencing the synaptic plasticity that occurs during postinjury recovery processes. To test this hypothesis, we documentedCOII mRNA expression and complex IV (cytochrome c oxidase) functional activity at 7 days postinjury, focusing on the long-term postinjury period mostclosely associated with synaptic reorganization. Both central fluid percussion TBI and combined TBI and bilateral entorhinal cortical lesion were examined. At 7 days survival, differential display, RT-PCR, and Northern blot analysis of hippocampal RNA from both TBI and combined insult models showeda significant induction of COII mRNA. This long-term elevation in COII gene expression was supported by increases in COII immunobinding. By contrast,cytochrome oxidase histochemical activity within tissue sections from injured brains suggested a reduction of complex IV activity within the TBI cases, but not within animals subjected to the combined insult. These differences in cytochrome c oxidase activity were supported by in vitro assay of complex IV using cerebral cortical and hippocampal tissues. Our present results support the hypothesis that COH is selectively vulnerable to TBI and thatCOII differences may indicate the degree of metabolic dysfunction induced by different pathologies. Taken together, such data will better define the role of metabolic function in long-term recovery after TBI.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 18/01/20 alle ore 14:04:42