Calcium mobilization evoked by amyloid β-protein involves inositol 1,4,5-trisphosphate production in human platelets

被引：19

作者：

Ishikawa, H

Ozawa, H

Saito, T

Takahata, N

Takemura, H

机构：

[1] Sapporo Med Univ, Sch Med, Dept Neuropsychiat, Chuo Ku, Sapporo, Hokkaido 060, Japan

[2] Sapporo Med Univ, Sch Med, Dept Pharmacol, Chuo Ku, Sapporo, Hokkaido 060, Japan

[3] Sapporo Med Univ, Sch Hlth Sci, Dept Occupat Therapy, Chuo Ku, Sapporo, Hokkaido 060, Japan

来源：

LIFE SCIENCES | 1998年 / 62卷 / 08期

关键词：

amyloid beta-protein; Ca(2+) mobilization; phospholipase C; platelet; Alzheimer's disease; human;

D O I：

10.1016/S0024-3205(97)01169-7

中图分类号：

R-3 [医学研究方法]; R3 [基础医学];

学科分类号：

1001 ;

摘要：

We examined the effects of amyloid beta-protein (A beta) on Ca(2+) mobilization in human platelets. The addition of A beta fragments 25-35 (A beta 25-35) gradually increased the cytoplasmic free Ca(2+) concentration ([Ca(2+)](i)). After the maximum response, [Ca(2+)](i) decreased and then reached a sustained, higher level of [Ca(2+)](i). Similar effects were also observed with A beta 1-40, whereas 1-28, 12-28 and 31-35 did not affect the Ca(2+) response. In the absence of extracellular Ca(2+), A beta 25-35 caused a transient increase in [Ca(2+)](i), which returned to the resting level. U73122, a phospholipase C inhibitor, completely abolished Ca(2+) mobilization induced by thrombin and A beta 25-35. Furthermore, A beta enhanced the production of inositol 1,4,5-trisphosphate (IP(3)) in platelets. These findings suggest that Ca(2+) mobilization induced by A beta 25-35 is due to phospholipase C activation and IP(3) production.

引用

页码：705 / 713

页数：9

共 30 条

[1] PLATELETS ARE THE PRIMARY SOURCE OF AMYLOID BETA-PEPTIDE IN HUMAN BLOOD [J].