| Project/Area Number |
06672287
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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 |
Laboratory medicine
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| Research Institution | Hokkaido University School of Medicine |
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Principal Investigator |
MATSUNO Kazuhiko HOKKAIDO UNIVERSITY SCHOOL OF MEDICINE,DEPARTMENT OF LABORATORY MEDICINE,ASSOCIATE PROFESSOR, 医学部, 助教授 (70102332)
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| Project Period (FY) |
1994 – 1995
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| Project Status |
Completed (Fiscal Year 1995)
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| Budget Amount *help |
¥1,900,000 (Direct Cost: ¥1,900,000)
Fiscal Year 1995: ¥700,000 (Direct Cost: ¥700,000)
Fiscal Year 1994: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | Platelets / CD36 / Collagen / Calcium / LDL / Thrombin / CD62P / CD63 / CP62P / 血小板粘着 / 血小板凝集 |
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| Research Abstract |
We researched the expression of CD36 on human platelets in normal healthy subjects (n=130) and patients with various diseases (n=111). CD36 was positive in 123 healthy subjects (94.6%) and negative in 7 subjects (5.4%). This results are compatible that other authors in Japan have reported (negative ; 3-7%). We observed the tendency that there were two groups whose peak value of CD36 expression per one platelet was high and low in normal subjects. But there were various peak value in platelets of various patients. Thus we measured the expression of CD36 and GPIb (CD42b) on the patients1 platelets by the two color method of flow cytemetry (FCM), their peak ratio (CD36 to GPIb) was divided into high (CD36 hyperxpression) and low (CD36 hypoexpression) groups. Hyperlipidemia, hypertension, trasient ischemic attack (TIA), et al. were in high ratio group and idiopathic thrombocytopenic purpura (ITP) et al. were in low ratio group. There was no correlation between the peak value of CD36 expression and MPV.The expression of CD36 expression was increased by thrombin and collagen. Thus, CD36 expression may be concerned with the platelet activation than the volume of platelets. The anti-platelet antibodies might play a role for decreassing CD36 expression.
We observed effects of platelet aggregation or activation in oxidized LDL (ox-LDL), but in native LDL (n-LDL). Ox-LDL induced platelet aggregation and expression of CD62P (GMP-140) and CD63 on platelets in adequate dose and enhanced platelet aggregation induced by thrombin in lower dose. These effects were followed by increasing cytosolic free Ca^<2+>([Ca^<2+>]i). The anti-CD36 monoclonal antibody (MoAb) inhibited the binding of ox-LDL to platelets by about 50%. These results show that the platelet CD36 antigen may be one of the ox-LDL receptors on human platelets.
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