Tumor necrosis factor α augments amyloid β protein (25-35) induced apoptosis in human cells

被引:43
作者
Blasko, I
Schmitt, TL
Steiner, E
Trieb, K
Grubeck-Loebenstein, B
机构
[1] Austrian Acad Sci, Inst Biomed Aging Res, A-6020 Innsbruck, Austria
[2] Dept Surg, Innsbruck, Austria
关键词
Alzheimer's disease; amyloid beta protein; amyloid beta protein (25-35); apoptosis; cytokines; DU-145; kidney cells; SK-N-SH; tumor necrosis factor alpha; thyroid cells;
D O I
10.1016/S0304-3940(97)00845-8
中图分类号
Q189 [神经科学];
学科分类号
071006 ;
摘要
No information is yet available on the effect of tumor necrosis factor alpha (TNF alpha) on amyloid beta protein (A beta)-induced cytotoxicity in human cells. For this reason the induction of apoptosis by TNF alpha and A beta (25-35) was studied in primary cultures of human thyroid and kidney cells as well as in the neuroblastoma line SK-N-SH and in DU-145 cells. Apoptosis occurred in all cell types after A beta (25-35) treatment, but was markedly enhanced when TNF alpha was additionally present. This effect was less pronounced in transformed cell lines than in primary cultures, in which TNF alpha on its own was not cytotoxic. Apoptosis was still more prevalent under serum free culture conditions. The results demonstrate that TNF alpha may support the occurrence of A beta-mediated cell death and thus contribute to the development of pathological changes in Alzheimer's disease (AD). (C) 1997 Elsevier Science Ireland Ltd.
引用
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页码:17 / 20
页数:4
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