PrP fragment 106-126 is toxic to cerebral endothelial cells expressing PrPC

被引：39

作者：

Deli, MA

Sakaguchi, S

Nakaoke, R

Abrahám, CS

Takahata, H

Kopacek, J

Shigematsu, K

Katamine, S

Niwa, M

机构：

[1] Nagasaki Univ, Grad Sch Med Sci, Dept Pharmacol, Nagasaki 8528523, Japan

[2] Nagasaki Univ, Grad Sch Med Sci, Dept Neurosurg, Nagasaki 8528523, Japan

[3] Nagasaki Univ, Sch Med, Dept Pathol 2, Nagasaki 8528523, Japan

[4] Nagasaki Univ, Grad Sch Med Sci, Dept Mol Microbiol & Immunol, Nagasaki 8528523, Japan

[5] Hungarian Acad Sci, Biol Res Ctr, Inst Biophys, Mol Neurobiol Lab, H-6726 Szeged, Hungary

来源：

NEUROREPORT | 2000年 / 11卷 / 17期

关键词：

cellular prion protein; cerebral endothelial cells; pentosan polysulphate; PrP fragment 106-126; toxicity;

D O I：

10.1097/00001756-200011270-00064

中图分类号：

Q189 [神经科学];

学科分类号：

071006 ;

摘要：

A hydrophobic, fibrillogenic peptide fragment of human prion protein (PrP106-126) had in vitro toxicity to neurons expressing cellular prion protein (PrPC). In this study, we proved that primary cultures of mouse cerebral endothelial cells (MCEC) express PrPC. Incubation of MCEC with PrP106-126 (25-200 muM) caused a dose-dependent toxicity assessed by 3-(4,5dimethylthiazol-2-yl)-2,5-diphenyltetrazlium bromide (MTT) assay, lactate dehydrogenase release, bis-benzimide staining for nuclear morphology, and trypan blue exclusion test. Pentosan polysulphate (50-100 mug/ml), a drug effective in scrapie prophylaxis, dose-dependently attenuated the injury. MCEC cultures from mice homogenous for the disrupted PrP gene were resistant to the toxicity of PrP106-126. In conclusion, cerebral endothelium expressing PrPC may be directly damaged during spongiform encephalopathies. NeuroReport 11:3931-3936 (C) 2000 Lippincott Witliams & Wilkins.

引用

页码：3931 / 3936

页数：6

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