| Project/Area Number |
04671511
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| Research Category |
Grant-in-Aid for General Scientific Research (C)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | University of Tokyo |
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Principal Investigator |
HASHIMOTO Yoshiaki Medicine, Internal Medicine, Assistant Prof., 医学部(病), 助手 (40172879)
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| Co-Investigator(Kenkyū-buntansha) |
KINOSHITA Makoto Medicine, Internal Medicine, Assistant Fellow, 医学部(病), 医員 (70186295)
TOKUNAGA Kazuki Medicine, Internal Medicine, Assistant Fellow, 医学部(病), 医員
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| Project Period (FY) |
1992 – 1993
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| Project Status |
Completed (Fiscal Year 1993)
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| Budget Amount *help |
¥2,200,000 (Direct Cost: ¥2,200,000)
Fiscal Year 1993: ¥1,000,000 (Direct Cost: ¥1,000,000)
Fiscal Year 1992: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | platelet aggregation / ATP release / myosin light chain kinase / protein kinase C / wortmannin |
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| Research Abstract |
We examined the roles of the protein kinases in platelet aggregation and release.
<Methods>
1.Platelets : Platelet rich plasma and washed platelets were prepared from bloods of healthy volunteers.
2.Measurement of platelet responses : Platelet aggregation and ATP release were monitored using a CAF-100 Ca^<2+> analyzer. ATP release was measured by the luciferin-luciferase reaction.
<Results>
1.The roles of myosin light chain kinase.
The specific inhibitor of myosin light chain kinase wortmannin inhibited ADP-induced platelet aggregation with no effect on their shape change.
2.The roles of protein kinase C.
The specific inhibitor of protein kinase C PKC-I did not affect much U46619-induced platelet aggregation and ATP release. However the inhibition of platelet aggregation with GRGDS prevented ATP release in the presence of PKC-I.On the other hand, ATP release was not seen in the presence of PKC-I in washed platelets.
<Conclusion>
1.It was suggested that myosin light chain kinase activation is a prerequisite for ADP-induced platelet aggregation, but not for changes in their shape.
2.It was suggested that there are protein-kinase C-dependent and -independent mechanisms for ATP release by human platelets and that activation of the latter mechanism may depend on aggregation and plasma factors.
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