Activation of human microglia by fibrillar prion protein-related peptides is enhanced by amyloid-associated factors SAP and C1q

被引：21
|
作者：
Veerhuis, R
Boshuizen, RS
Morbin, M
Mazzoleni, G
Hoozemans, JJM
Langedijk, JPM
Tagliavini, F
Langeveld, JPM
Eikelenboom, P
机构：
[1] Vrije Univ Amsterdam, Ctr Med, Dept Pathol, NL-1007 MB Amsterdam, Netherlands
[2] Vrije Univ Amsterdam, Ctr Med, Dept Psychiat, Inst Clin & Expt Neurosci, NL-1007 MB Amsterdam, Netherlands
[3] Pepscan Syst BV, NL-8203 AB Lelystad, Netherlands
[4] Ist Nazl Neurol Carlo Besta, I-20133 Milan, Italy
[5] Cent Inst Anim Dis Control, NL-8203 AA Lelystad, Netherlands
[6] Univ Amsterdam, Acad Med Ctr, Dept Neurol, NL-1105 AZ Amsterdam, Netherlands
来源：
NEUROBIOLOGY OF DISEASE | 2005年 / 19卷 / 1-2期
关键词：
prion peptides; microglia; cytokines; C1q; SAP; fibrillarity; thioflavin; Creutzfeldt Jakob disease (CJD);
D O I：
10.1016/j.nbd.2005.01.005
中图分类号：
Q189 [神经科学];
学科分类号：
071006 ;
摘要：
Complement activation products C1q and C3d, serum amyloid P component (SAP) and activated glial cells accumulate in amyloid deposits of conformationally changed prion protein (PrPSc) in Creutzfeldt-Jakob disease, Gerstmann-Straussier-Scheinker disease and scrapie-infected mouse brain. Biological properties, including the potential to activate microglia, relate to prion (PrP) peptide fibrillogenic abilities. We investigated if SAP and C1q influence the fibrillogenic properties of human and mouse PrP peptide and concomitantly their stimulatory effects on human microglia in vitro. PrP-peptide induced microglial IL-6 and TNF-alpha, release significantly increased in the presence of SAP and C1q. Also, SAP and C1q enhanced PrP-peptide fibril formation as revealed by electron microscopy and thioflavin S-based quantitative assays. This suggests that SAP and C1q contribute to fibrillar state-dependent cellular effects of PrP. Combined, ultrastructural and thioflavin assays, together with microglial cytokine release measurements, provide a test system to screen potential, fibrillarity impeding therapeutics for prion disease. (c) 2005 Elsevier Inc. All rights reserved.
引用
收藏
页码：273 / 282
页数：10
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