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Titolo:
beta-VLDL protects against A beta(I-42) and apoE toxicity in human SH-SY5Yneuroblastoma cells
Autore:
Cedazo-Minguez, A; Huttinger, M; Cowburn, RF;
Indirizzi:
Karolinska Inst, NEUROTEC, Geriatr Med Sect, NOVUM, S-14186 Huddinge, Sweden Karolinska Inst Huddinge Sweden S-14186 NOVUM, S-14186 Huddinge, Sweden Univ Vienna, Dept Med Chem, A-1010 Vienna, Austria Univ Vienna Vienna Austria A-1010 Dept Med Chem, A-1010 Vienna, Austria
Titolo Testata:
NEUROREPORT
fascicolo: 2, volume: 12, anno: 2001,
pagine: 201 - 206
SICI:
0959-4965(20010212)12:2<201:BPAABA>2.0.ZU;2-Q
Fonte:
ISI
Lingua:
ENG
Soggetto:
HIGH-DENSITY-LIPOPROTEIN; APOLIPOPROTEIN-E; NEURITE OUTGROWTH; AMYLOID PEPTIDE; NEUROTOXICITY; SECRETION; SURVIVAL; DISEASE; BRAIN; FORM;
Keywords:
Alzheimer's disease; beta-amyloid; apolipoprotein E; cytotoxicity; lipoproteins;
Tipo documento:
Article
Natura:
Periodico
Settore Disciplinare:
Life Sciences
Citazioni:
25
Recensione:
Indirizzi per estratti:
Indirizzo: Cowburn, RF Karolinska Inst, NEUROTEC, Geriatr Med Sect, NOVUM, Plan 4,KFC, S-14186 Huddinge, Sweden Karolinska Inst Plan 4,KFC Huddinge Sweden S-14186 ge, Sweden
Citazione:
A. Cedazo-Minguez et al., "beta-VLDL protects against A beta(I-42) and apoE toxicity in human SH-SY5Yneuroblastoma cells", NEUROREPORT, 12(2), 2001, pp. 201-206

Abstract

The toxic effects of beta -amyloid (A beta) (1-42), apolipoprotein E (apoE) isoforms, and apoE/A beta complexes were studied in human SH-SY5Y neuroblastoma cells and fibroblasts using MTT reduction. In SH-SY5Y cells, A beta (1-42) gave time-dependent toxicity over 2-48 h, which was reduced by co-incubation with rabbit beta -very low density lipoproteins (beta -VLDL). Human recombinant apoE3 and E4 isoforms were also toxic by themselves and also potentiated A beta effects when used alone, but not when associated with beta -VLDL. None of the treatments were toxic to human fibroblasts. These results suggest that beta -VLDL has a protective role on A beta -induced neurotoxicity and that the status of apoE or the conformation of lipoprotein containing apoE particles may be important for determining the contribution ofapoE to neurodegeneration. NeuroReport 12:201-206 (C) 2001 Lippincott Williams & Wilkins.

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Documento generato il 06/04/20 alle ore 04:49:27