Study on a new release mechanism abnormality (unresponsiveness to thromboxane A_2) of platelet
| Project/Area Number |
61480257
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| Research Category |
Grant-in-Aid for General Scientific Research (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Hematology
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| Research Institution | Niigata University |
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Principal Investigator |
HATTORI Akira First Department of Internal Medicine, 医学部, 助教授 (10018731)
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| Co-Investigator(Kenkyū-buntansha) |
KOIKE Tadashi First Department of Internal Medicine, 医学部付属病院, 助手 (30170161)
TAKAHASHI Hoyu First Department of Internal Medicine, 医学部付属病院, 助手 (70163285)
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| Project Period (FY) |
1986 – 1987
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| Project Status |
Completed (Fiscal Year 1988)
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| Budget Amount *help |
¥3,600,000 (Direct Cost: ¥3,600,000)
Fiscal Year 1987: ¥500,000 (Direct Cost: ¥500,000)
Fiscal Year 1986: ¥3,100,000 (Direct Cost: ¥3,100,000)
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| Keywords | Platelet dysfunction / Ca^<++> mobilization / unresponsiveness to thromboxane A_2 / 放出機構障害 / 血小板 / 出血性素因 / 放出反応 / Ca2+動員 / Aequorin 08711794000600長山礼三: 第28回日本臨床血液学会総会抄録集. 281 (1986) / 【Ca^(++)】動員 / Aequorin |
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| Research Abstract |
In order to clarify the mechanism of defect in a new type of platelet release mechanism abnormality reported by us in 1980-1981, intracellular Ca^<++>,[Ca^<++>]i, mobilization was analysed in cases of thrombin, A23187, stable thromboxane analog SAT_2 or arachidonate-induction using aequorin loading method. In presence of L mM Ca^<++>, patient (P) platelets showed normal [Ca^<++>]i elevation (influx and intracellular mobilization) in response to thrombin, but suppressed one to low concentration of A23187 or STA_2. The decreased mobilization in absence of Ca^<++> was enhanced to normal by addition of 2mM Ca^<++> or by adrenalin potentiation. TMB-8 which caused reduced aggregation similar to P platelets in normal platelets was not sensitive to adrenalin potentiation. Various but slight degree of abnormalities in [Ca^<++>]i mobilization were found in Bernard-Soulier syndrome, cyclooxygenase deficiency, and Hermansky-Pudlak syndrome, suggestkng different characters of Ca^<++> mobilization measured by present method. In conclusion P platelets were partially defective in Ca^<++> mobilization (probably Ca influx) in responses to A23187 or STA_2, and different from TMB-8 treated normal paltelets. Closer relation between[Ca^<++>]i mobilization and aggregation or release in various agonists is neccessary to be investigated.
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Report
(3 results)
Research Products
(13 results)
