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Titolo:
GDNF protects against aluminum-induced apoptosis in rabbits by upregulating Bcl-2 and Bcl-X-L and inhibiting mitochondrial bax translocation
Autore:
Ghribi, O; Herman, MM; Forbes, MS; DeWitt, DA; Savory, J;
Indirizzi:
Univ Virginia, Dept Pathol, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 Charlottesville, VA 22908 USA Univ Virginia, Dept Biochem, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 Charlottesville, VA 22908 USA Univ Virginia, Dept Mol Genet, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 Charlottesville, VA 22908 USA NIMH, IRP, NIH, Bethesda, MD 20892 USA NIMH Bethesda MD USA 20892NIMH, IRP, NIH, Bethesda, MD 20892 USA Liberty Univ, Dept Biol & Chem, Lynchburg, VA 24506 USA Liberty Univ Lynchburg VA USA 24506 Biol & Chem, Lynchburg, VA 24506 USA
Titolo Testata:
NEUROBIOLOGY OF DISEASE
fascicolo: 5, volume: 8, anno: 2001,
pagine: 764 - 773
SICI:
0969-9961(200110)8:5<764:GPAAAI>2.0.ZU;2-Z
Fonte:
ISI
Lingua:
ENG
Soggetto:
PERMEABILITY TRANSITION PORE; NEUROTROPHIC FACTOR; CYTOCHROME-C; BRAIN INJURY; INDUCED NEURODEGENERATION; ENDOPLASMIC-RETICULUM; ALZHEIMERS-DISEASE; OXIDATIVE STRESS; CELL; ACTIVATION;
Keywords:
cytochrome c; Bax; Bcl-2; Bcl-X-L; caspase-3; GDNF; aluminum; endoplasmic reticulum;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
34
Recensione:
Indirizzi per estratti:
Indirizzo: Ghribi, O Univ Virginia, Dept Pathol, Charlottesville, VA 22908 USA Univ Virginia Charlottesville VA USA 22908 sville, VA 22908 USA
Citazione:
O. Ghribi et al., "GDNF protects against aluminum-induced apoptosis in rabbits by upregulating Bcl-2 and Bcl-X-L and inhibiting mitochondrial bax translocation", NEUROBIOL D, 8(5), 2001, pp. 764-773

Abstract

Direct (intracisternal) injection of aluminum complexes into rabbit brain results in a number of similarities with the neuropathological and biochemical changes observed in Alzheimer's disease and provides the opportunity toassess early events in neurodegeneration. This mode of administration induces cytochrome c release from mitochondria, a decrease in Bcl-2 in both mitochondria and endoplasmic reticulum, Bax translocation into mitochondria, activation of caspase-3, and DNA fragmentation. Coadministration of glial cell neuronal-derived factor (GDNF) inhibits these Bcl-2 and Bax changes, upregulates Bcl-X-L, and abolishes the caspase-3 activity. Furthermore, treatment with GDNF dramatically inhibits apoptosis, as assessed by the TUNEL technique for detecting DNA damage. Treatment with GDNF may represent a therapeutic strategy to reverse the neuronal death associated with Alzheimer's disease and may exert its effect on apoptosis-regulatory proteins. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 23/09/20 alle ore 12:56:07