Tumor necrosis factor-α reduces beta-amyloid accumulation primarily by lowering cellular prion protein levels in a brain endothelial cell line

被引：5

作者：

Yasutaka, Yuki ^{[2
]}

Watanabe, Takuya ^{[1
]}

Nakashima, Akio ^{[2
]}

Matsumoto, Junichi ^{[2
]}

Futagami, Koujiro ^{[2
]}

Yamauchi, Atsushi ^{[1
]}

Kataoka, Yasufumi ^{[1
]}

机构：

[1] Fukuoka Univ, Fac Pharmaceut Sci, Dept Pharmaceut Care & Hlth Sci, Jonan Ku, Fukuoka 8140180, Japan

[2] Fukuoka Univ, Fac Pharmaceut Sci, Dept Pharmaceut & Hlth Care Management, Jonan Ku, Fukuoka 8140180, Japan

来源：

FEBS LETTERS | 2015年 / 589卷 / 02期

基金：

日本学术振兴会;

关键词：

Prion protein; Beta-amyloid; Brain endothelial cell; Tumor necrosis factor-alpha; Alzheimer's disease; P-GLYCOPROTEIN; TRANSPORT ACTIVITY; BARRIER; EXPRESSION; DISEASE; MODEL; BILE;

D O I：

10.1016/j.febslet.2014.12.007

中图分类号：

Q5 [生物化学]; Q7 [分子生物学];

学科分类号：

071010 ; 081704 ;

摘要：

Disruption of beta-amyloid (Ab) transport across the blood-brain barrier is thought to cause Ab accumulation in the brain, thus leading to the development of Alzheimer's disease (AD). As AD patients show increased serum tumor necrosis factor-alpha (TNF alpha) levels, we examined the effect of TNF alpha on the function and expression of Ab transport-related proteins including cellular prion protein (PrPC) in the mouse brain microvascular endothelial cell line MBEC4. TNF alpha decreased PrPC levels and intracellular radiolabeled Ab. Similarly, anti-prion protein antibody also decreased radiolabeled Ab. These results suggest that TNF alpha lowers PrPC levels, which in turn, reduces Ab in the brain endothelium. (C) 2014 Federation of European Biochemical Societies. Published by Elsevier B. V. All rights reserved.

引用

收藏

页码：263 / 268

页数：6

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