| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2013: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2012: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
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| Outline of Final Research Achievements |
The present research project yielded the following achievements regarding the role of thrombin receptor in the pathogenesis and progression of atherosclerosis:1. Thrombin receptor PAR1 induces the phosphorylation of myosin light chain, thereby increasing the permeability of endothelial cells. 2. The di-phosphorylation of myosin light chain and the actin filament formation at the cell periphery play a key role for the increase in endothelial permeability.
3. The present research established the cellular model, in which the desensitization mechanism for the thrombin receptor is impaired. Namely, the cells exhibited sustained, repetitive and irreversible response to thrombin receptor agonists. These phenomenon are indicators for impairment of receptor desensitization. 4. Oxidative stress and extracellular signal-regulated protein kinase (ERK) play a critical role for the impairment of receptor desensitization.
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