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1993 Fiscal Year Final Research Report Summary

Roles of the protein kinases on platelet functions

Research Project

Project/Area Number 04671511
Research Category

Grant-in-Aid for General Scientific Research (C)

Allocation TypeSingle-year Grants
Research Field Hematology
Research InstitutionUniversity of Tokyo

Principal Investigator

HASHIMOTO Yoshiaki  Medicine, Internal Medicine, Assistant Prof., 医学部(病), 助手 (40172879)

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
Project Period (FY) 1992 – 1993
Keywordsplatelet aggregation / ATP release / myosin light chain kinase / protein kinase C / wortmannin
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.

  • Research Products

    (6 results)

All Other

All Publications (6 results)

  • [Publications] Yoshiaki Hashimoto et al: "Two thrombin-activated Ca^<2+> channels in human platelets" J.Biol Chem. 267. 17078-17081 (1992)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yoshiaki Hashimoto et al: "Ca^<2+> entry pathways activated by the tumor promoter thapsigargin in human platelets" Biochim.Biophys Acta.1220. 37-41 (1993)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yoshiaki Hashimoto et al: "Protein kinase C-dependent and independent mechanisms of clense granule exocytosis by human platelets" Biochim.Biophys Acta in press.(1994)

    • Description
      「研究成果報告書概要(和文)」より
  • [Publications] Yoshiaki Hashimoto et al.: "Two thombin-activated Ca^<2+> channels in human platelets" J.Biol.Chem.267. 17078-17081 (1992)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yoshiaki Hashimoto et al.: "Ca^<2+> entry pathways activated by the tumor promoter thapsigargin in human platelets." Biochim.Biophys.Acta. 1220. 37-41 (1993)

    • Description
      「研究成果報告書概要(欧文)」より
  • [Publications] Yoshiaki Hashimoto et al.: "Protein kinase C-dependent and -independent mechchanisms of dense granule exocytosis by human platelets." Biochim.Biophys.Acta. (in press).

    • Description
      「研究成果報告書概要(欧文)」より

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Published: 1995-03-27  

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