| Project/Area Number |
03671202
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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 | The Tokyo Metropolitan Institute of Medical Science, Department of Cardiovascular Research |
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Principal Investigator |
YAMAMOTO Naomasa The Tokyo Metropolitan Institute of Medical Science, Department of Cardiovascular Research, Scientist, 循看器病研究部門, 研究員 (50150884)
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| Co-Investigator(Kenkyū-buntansha) |
TANOUE Kenjiro The Tokyo Metropolitan Institute of Medical Science, Department of Cardiovascula, 循環器病研究部門, 部長 (30014137)
SAKURADA Hitoshi The Tokyo Metropolitan Institute of Medical Science, Department of Clinical Gene, 臨床遺伝病学研究部門, 室長 (60114493)
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| Project Period (FY) |
1991 – 1992
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| Project Status |
Completed (Fiscal Year 1992)
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| Budget Amount *help |
¥2,000,000 (Direct Cost: ¥2,000,000)
Fiscal Year 1992: ¥800,000 (Direct Cost: ¥800,000)
Fiscal Year 1991: ¥1,200,000 (Direct Cost: ¥1,200,000)
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| Keywords | GPIV / GPIV-deficiency / Platelet aggregation / Monocytes / Type I-deficiency / Type II-deficiency / Iso-antibody / PCR / type Iの欠損者 |
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| Research Abstract |
Using both a binding assay of ^<125>I-OKM5 against CD36 and rabbit anti-GPIV antibody-induced aggregation, platelets from 16 individuals out of healthy 354 Japanese were found to be GPIV-deficient. Monocytes from these platelet-GPIV deficient individuals were analyzed by flowcytometry. GPIV was absent on the monocytes from two of the individuals (type I-deficiency), while it was preset on the monocytes from the remaining 14 platelet-GPIV deficient individuals. Anti-GPIV antibody was detected in the serum from the one of the type I-deficient individuals, Na.S who had ever delivered three children. She is health and have never bleeding problems. This suggested that type I-deficient individuals may be at high risk to develop an iso-anti-GPIV antibody upon blood transfusion or pregnancy.
The platelet aggregations of GPIV deficient platelets induced by collaren, ADP, arachidonic acid, and thrombin were normal. Analysis of GPIV-mRNA in type II-deficiency using PCR amplification revealed the presence of normal size of mRNA (1.6 kb). However, in 79 position, C-A change was observed, and just after 1632 position, four nuclear bases, AGTA were inserted. These changes in GPIV mRNA appeared to be polymorphic, because GPIV was expressed normally on the monocytes surface from type II deficient individuals. In conclusion, our finding of two types of GPIV-deficiency is very important to clarify the mechanism of GPIV-deficiency and to perform genomic analysis of GPIV in near future.
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