1991 Fiscal Year Final Research Report Summary
Intracellular signal transduction and phospholipid metabolism in platelets and neutrophils
| Project/Area Number |
01570680
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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 | Kyoto University (1990-1991)
福井医科大学 (1989) |
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Principal Investigator |
TAKAYAMA Hiroshi Kyoto University. Dept. of Medicine, Assistant, 医学部, 助手 (10197220)
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| Project Period (FY) |
1989 – 1991
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| Keywords | Signal transduction / Platelet / Phospholipid / Protein phosphorylation |
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| Research Abstract |
Our new findings during this research support are as follows. 1. Activation of protein kinase C before stimulation of thrombin or A23187 enhances release of arachidonate from platelet membrane. 2. Indomethacin inhibits transfer of arachidonate into phosphatidyl-ethanolamine as well as arachidonate release. 3. A23187 or thrombin can stimulate protein-tyrosine phosphorylation of platelets. 4. Thrombin-induced protein-tyrosine phosphorylation is not dependent on GTP-binding protein, intra-and extra-cellular Ca^<2+>, binding of fibrinogen to GPllbllla, thromboxane A_2 formation and released ADP. 5. A23187 or thromboxane A_2 evokes protein-tyrosin phosphorylation of platelets through increase of intracellular Ca^<2+> via unknown mechanisms. 6. A23187-induced protein-tyrosine phosphorylation may be involved in platelet aggregation but not in secretion. 7. There may be synergistic stimulation of protein-tyrosine phosphorylation between intracellular Ca^<2+> and protein kinase C.
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