β-VLDL protects against Aβ(I-42) and apoE toxicity in human SH-SY5Y neuroblastoma cells

被引:22
作者
Cedazo-Mínguez, A
Hüttinger, M
Cowburn, RF
机构
[1] Karolinska Inst, NEUROTEC, Geriatr Med Sect, NOVUM, S-14186 Huddinge, Sweden
[2] Univ Vienna, Dept Med Chem, A-1010 Vienna, Austria
关键词
Alzheimer's disease; beta-amyloid; apolipoprotein E; cytotoxicity; lipoproteins;
D O I
10.1097/00001756-200102120-00006
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
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 of apoE to neurodegeneration. NeuroReport 12:201-206 (C) 2001 Lippincott Williams & Wilkins.
引用
收藏
页码:201 / 206
页数:6
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