Human platelet calcium mobilisation in response to β-amyloid (25-35):: buffer dependency and unchanged response in Alzheimer's disease

被引：10
|
作者：
Hedin, HLM [1 ]
Eriksson, S
Fowler, CJ
机构：
[1] Umea Univ, Dept Pharmacol & Clin Neurosci, SE-90187 Umea, Sweden
[2] Umea Univ, Dept Community Med & Rehabil, SE-90187 Umea, Sweden
来源：
NEUROCHEMISTRY INTERNATIONAL | 2001年 / 38卷 / 02期
关键词：
Alzheimer's disease; U-73122; amyloid beta peptides; platelets; serotonin;
D O I：
10.1016/S0197-0186(00)00068-1
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：
In the present study, the effects of beta -amyloid (25-35) (A beta (25-35)) upon calcium signalling by the human platelet has been investigated. When assays were conducted using HEPES buffers, A beta (25-35), but not the inactive peptide A beta (35-25), produced a robust increase in intracellular calcium that remained after removal of extracellular calcium but was abolished by the phospholipase C inhibitor U-73122. There was no significant difference bt tween the calcium response to A beta (25-35) in platelets from patients with Alzheimer's disease and from age-matched controls. In contrast to the robust effects on calcium mobilisation in HEPES buffers, very little calcium response to A beta (25-35) was seen when Krebs (pH 7.8) buffer was used. (C) 2001 Elsevier Science Ltd. All rights reserved.
引用
收藏
页码：145 / 151
页数：7
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