Intracellular pathways involved in TNF-α and superoxide anion release by Aβ(1-42)-stimulated primary human macrophages

被引：15

作者：

Smits, HA ^{[1
]}

de Vos, NM ^{[1
]}

Wat, JWY ^{[1
]}

van der Bruggen, T ^{[1
]}

Verhoef, J ^{[1
]}

Nottet, HSLM ^{[1
]}

机构：

[1] Univ Utrecht, Med Ctr Utrecht, Eijkman Winkler Inst, Sect Neuroimmunol, NL-3584 CX Utrecht, Netherlands

来源：

JOURNAL OF NEUROIMMUNOLOGY | 2001年 / 115卷 / 1-2期

关键词：

Alzheimer's disease; beta-amyloid; kinases; signal transduction; TNF-alpha;

D O I：

10.1016/S0165-5728(01)00254-5

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

In this study, the intracellular signal transduction pathways leading to the production of TNF-alpha and superoxide anions by amyloid-beta -stimulated primary human monocyte-derived macrophages was investigated. Using Western blotting and specific inhibitors it is shown that both ERK 1/2 and p38 MAPK signal transduction pathways as well as PKC are involved in the amyloid-beta -stimulated superoxide anion production. In contrast. only ERK 1/2 MAPK seems to be involved in TNF-alpha production: questioning the connection between PKC and ERK 1/2 activation. Our results suggest the use of ERK 1/2 MAPK inhibitors in the prevention of macrophage activation in the context of Alzheimer's disease. (C) 2001 Elsevier Science B.V. All rights reserved.

引用

页码：144 / 151

页数：8

共 38 条

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