Project/Area Number |
23592249
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Anesthesiology/Resuscitation studies
|
Research Institution | Gifu University |
Principal Investigator |
AKAMATSU Shigeru 岐阜大学, 医学(系)研究科(研究院), 非常勤講師 (20167828)
|
Co-Investigator(Kenkyū-buntansha) |
KOZAWA Osamu 岐阜大学, 医学系研究科, 教授 (90225417)
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,070,000 (Direct Cost: ¥3,900,000、Indirect Cost: ¥1,170,000)
Fiscal Year 2013: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2012: ¥1,430,000 (Direct Cost: ¥1,100,000、Indirect Cost: ¥330,000)
Fiscal Year 2011: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
|
Keywords | 心血管 / 血栓 / 血小板 / 凝固 / 綿溶 / 線溶 / トロンビン / トロンボモジュリン / トロンボポエチン / PAI-1 / 侵害刺激 / 全身性炎症反応症候群 / アンチトロンビン / PAI-1 / 凝固障害 |
Research Abstract |
We previously demonstrated that ristocetin, an activator of GPIb/IX/V, induces release of sCD40L via TXA2 production from human platelets. In the present study, we investigated the effect of antithrombin-III (AT-III), an anticoagulant, on the ristocetin-induced GPIb/IX/V activation in human platelets. AT-III inhibited ristocetin-stimulated platelet aggregation. The ristocetin-induced production of 11-dehydro-TXB2, a stable metabolite of TXA2, and the release of sCD40L were suppressed by AT-III. AT-III also reduced the ristocetin-stimulated secretion of PDGF-AB. AT-III failed to affect the U46619-, a TP receptor agonist, induced levels of p38 MAP kinase phosphorylation or sCD40L release. AT-III reduced the binding of SZ2, a monoclonal antibody to the sulfated sequence in the alpha-chain of GPIb, to the ristocetin-stimulated platelets. These results strongly suggest that AT-III reduce ristocetin-stimulated release of sCD40L due to inhibiting TXA2 production in human platelets.
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