| Project/Area Number |
25860801
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | Osaka University (2014)
National Cardiovascular Center Research Institute (2013) |
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Principal Investigator |
TASHIMA Yuko 大阪大学, 微生物病研究所, 助教 (10423104)
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| Project Period (FY) |
2013-04-01 – 2015-03-31
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| Project Status |
Completed (Fiscal Year 2014)
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| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
Fiscal Year 2013: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Keywords | プラスミノーゲン / 線溶 / 静脈血栓症 / 肺塞栓 / プラスミノーゲン栃木変異 |
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| Outline of Final Research Achievements |
Plasminogen (Plg) is a precursor of a serine protease, plasmin to degrade fibrin fiber in blood clot. Plg-A620T mutation previously named as Plg-Tochigi was identified in Japanese patients with deep venous thrombosis. We investigated whether the homozygous Plg-A622T mutation corresponding to human Plg-Tochigi caused serious thrombosis in mice. Compared to wild-type mice, Plg-A620T mice showed the lower activity of plasmin, but did not affect wound healing unlike Plg-KO mice. Plg-Tochigi mutation did not significantly affect the severity of thrombogenesis under three different experimental thrombosis models: a middle cerebral artery occlusion model of ischemia-reperfusion injury, acute pulmonary embolism model by injection of recombinant human tissue factor via inferior vena cava, and inferior vena cava thrombosis model with electrolytic stimulation. In conclusion, homozygous Plg-Tochigi mutation showed reduced enzymatic activity of plasmin but did not cause severe thrombosis in mice.
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