Catalogo Articoli (Spogli Riviste)

OPAC HELP

Titolo:
Differential neuroprotection from human heat shock protein 70 overexpression in in vitro and in vivo models of ischemia and ischemia-like conditions
Autore:
Lee, JE; Yenari, MA; Sun, GH; Xu, LJ; Emond, MR; Cheng, DY; Steinberg, GK; Giffard, RG;
Indirizzi:
Stanford Univ, Dept Anesthesia, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 pt Anesthesia, Stanford, CA 94305 USA Stanford Univ, Dept Neurosurg, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 ept Neurosurg, Stanford, CA 94305 USA Stanford Univ, Dept Neurol, Stanford, CA 94305 USA Stanford Univ StanfordCA USA 94305 , Dept Neurol, Stanford, CA 94305 USA Stanford Univ, Stanford Stroke Ctr, Stanford, CA 94305 USA Stanford Univ Stanford CA USA 94305 rd Stroke Ctr, Stanford, CA 94305 USA
Titolo Testata:
EXPERIMENTAL NEUROLOGY
fascicolo: 1, volume: 170, anno: 2001,
pagine: 129 - 139
SICI:
0014-4886(200107)170:1<129:DNFHHS>2.0.ZU;2-0
Fonte:
ISI
Lingua:
ENG
Soggetto:
OXYGEN-GLUCOSE DEPRIVATION; STRESS-INDUCED APOPTOSIS; FOCAL CEREBRAL-ISCHEMIA; CULTURED NEURONS; TRANSGENIC MICE; MESSENGER-RNA; TRANSIENT ISCHEMIA; GLUTAMATE TOXICITY; MYOGENIC CELLS; GERBIL BRAIN;
Keywords:
heat shock protein 70; stress response; oxidative stress; transgenic mouse; cerebral ischemia;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
58
Recensione:
Indirizzi per estratti:
Indirizzo: Lee, JE Yonsei Univ, Coll Med, Dept Anat, Seodaemun Ku, 134 Shinchon Dong,Seoul 120752, South Korea Yonsei Univ 134 Shinchon Dong Seoul South Korea120752 outh Korea
Citazione:
J.E. Lee et al., "Differential neuroprotection from human heat shock protein 70 overexpression in in vitro and in vivo models of ischemia and ischemia-like conditions", EXP NEUROL, 170(1), 2001, pp. 129-139

Abstract

We previously showed that overexpressing the 70-kDa inducible heat shock protein in primary astrocyte cultures and in a rodent stroke model using viral vectors resulted in protection from ischemia and ischemia-like injury. However, viral transfection could potentially provoke a stress response itself; therefore, we examined whether transgenic mice constitutively expressing human heat shock protein 70 were protected from ischemic insults. Astrocyte cultures from brains of heat shock protein 70 transgenic mice were resistant to hydrogen peroxide injury in a dose-dependent fashion, but were lessresistant to hypoglycemia and oxygen-glucose deprivation. Because hydrogenperoxide exposure and glucose deprivation are partially dependent on glutathione levels, we determined whether heat shock protein 70 transgenic cultures had altered glutathione levels under normal growth conditions, However,there was no significant difference in glutathione levels between heat shock protein 70 transgenic and wildtype astrocytes. Hippocampal, but not cortical neuron cultures from these same transgenic mice were also protected against oxygen-glucose deprivation and glutamate toxicity. In an in vivo model of permanent focal cerebral ischemia, there was no significant differencein infarct size assessed 24 h post-insult, These results suggest that heatshock protein 70 protects against some but not all kinds of central nervous system injury. The protective effects may be related to the nature and severity of the insults, as well as subpopulations of brain cells and dose-dependent effects of HSP70 overexpression. (C) 2001 Academic Press.

ASDD Area Sistemi Dipartimentali e Documentali, Università di Bologna, Catalogo delle riviste ed altri periodici
Documento generato il 27/09/20 alle ore 05:44:01