Relationship between β-AP peptide aggregation and microglial activation

被引:35
作者
Casal, C
Serratosa, J
Tusell, JM
机构
[1] IDIBAPS, CSIC, Inst Invest Biomed Barcelona, Dept Pharmacol & Toxicol, E-08036 Barcelona, Spain
[2] IDIBAPS, CSIC, Inst Invest Biomed Barcelona, Dept Neurochem, E-08036 Barcelona, Spain
关键词
beta-amyloid peptide aggregatiom; microglial activation; microglial proliferation; beta-amyloid peptide toxicity;
D O I
10.1016/S0006-8993(01)03362-5
中图分类号
Q189 [神经科学];
学科分类号
071006 [神经生物学];
摘要
We compared the relationship between the state of aggregation of two peptides (beta-AP 25-35 and beta-AP 1-42) and microglial activation, After 7 days at 37 degreesC beta-AP 25-35 was in an amorphous state and did not activate microglial cells. In the same conditions, aggregated beta-AP 1-42 activated these cells and caused changes in microglial ramification, increasing the proliferation index and inducing tumor necrosis factor alpha (TNF alpha) release. Neither peptide induced a release of nitric oxide (NO). As the toxicity of beta-AP peptides in cell culture is associated with the formation of amyloid fibrils. we also examined the toxicity of both peptides in microglial cell cultures and in PC 12 cell cultures. The results Suggest that the two beta-AP fragments studied have similar neurotoxic effects but different pro-inflammatory activities. (C) 2002 Elsevier Science B.V. All rights reserved.
引用
收藏
页码:76 / 84
页数:9
相关论文
共 32 条
[1]
BETA-AMYLOID STIMULATES GLIAL-CELLS INVITRO TO PRODUCE GROWTH-FACTORS THAT ACCUMULATE IN SENILE PLAQUES IN ALZHEIMERS-DISEASE [J].
ARAUJO, DM ;
COTMAN, CW .
BRAIN RESEARCH, 1992, 569 (01) :141-145
[2]
Immunological aspects of microglia: relevance to Alzheimer's disease [J].
Benveniste, EN ;
Nguyen, VT ;
O'Keefe, GM .
NEUROCHEMISTRY INTERNATIONAL, 2001, 39 (5-6) :381-391
[3]
TUMOR-NECROSIS-FACTOR-ALPHA POTENTIATES GLUTAMATE NEUROTOXICITY IN HUMAN FETAL BRAIN-CELL CULTURES [J].
CHAO, CC ;
HU, SX .
DEVELOPMENTAL NEUROSCIENCE, 1994, 16 (3-4) :172-179
[4]
Insights into the neurodegenerative process of Alzheimer's disease: a role for mononuclear phagocyte-associated inflammation and neurotoxicity [J].
Cotter, RL ;
Burke, WJ ;
Thomas, VS ;
Potter, JF ;
Zheng, JL ;
Gendelman, HE .
JOURNAL OF LEUKOCYTE BIOLOGY, 1999, 65 (04) :416-427
[5]
CSAL C, 2001, BRAIN RES, V902, P101
[6]
CONTROL OF ASTROCYTOSIS BY INTERLEUKIN-1 AND TRANSFORMING GROWTH-FACTOR-BETA-1 IN HUMAN BRAIN [J].
DACUNHA, A ;
JEFFERSON, JJ ;
TYOR, WR ;
GLASS, JD ;
JANNOTTA, FS ;
VITKOVIC, L .
BRAIN RESEARCH, 1993, 631 (01) :39-45
[7]
MICROGLIA AND CYTOKINES IN NEUROLOGICAL DISEASE, WITH SPECIAL REFERENCE TO AIDS AND ALZHEIMERS-DISEASE [J].
DICKSON, DW ;
LEE, SC ;
MATTIACE, LA ;
YEN, SHC ;
BROSNAN, C .
GLIA, 1993, 7 (01) :75-83
[8]
Fujita H, 1996, GLIA, V18, P269, DOI 10.1002/(SICI)1098-1136(199612)18:4<269::AID-GLIA2>3.0.CO
[9]
2-T
[10]
α-MSH peptides inhibit production of nitric oxide and tumor necrosis factor-α by microglial cells activated with β-amyloid and interferon γ [J].
Galimberti, D ;
Baron, P ;
Meda, L ;
Prat, E ;
Scarpini, E ;
Delgado, R ;
Catania, A ;
Lipton, JM ;
Scarlato, G .
BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 1999, 263 (01) :251-256