| Budget Amount *help |
¥4,680,000 (Direct Cost: ¥3,600,000、Indirect Cost: ¥1,080,000)
Fiscal Year 2018: ¥1,040,000 (Direct Cost: ¥800,000、Indirect Cost: ¥240,000)
Fiscal Year 2017: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2016: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
In this study, we analyzed the effects of thrombotic molecules and their gene mutations on the pathogenesis of thrombosis using genetically modified mice established so far. The coexistence of the plasminogen-A622T mutation did not aggravate the thrombotic tendency caused by the protein S-K196E mutation. ADAMTS13 suppressed excessive neutrophil infiltration in the innate immune response. Extracellular signal-regulated kinase in platelets was essential for initiation and maintenance of thrombus formation. Protein kinase A in platelets inhibited thrombus formation only in the early phase. The integrin αIIb-R990W mutation induced constitutive activation of αIIbβ3 on platelets, but simultaneously reduced the expression of αIIbβ3 to cause impaired platelet aggregation.
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