| Budget Amount *help |
¥5,330,000 (Direct Cost: ¥4,100,000、Indirect Cost: ¥1,230,000)
Fiscal Year 2014: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2013: ¥2,210,000 (Direct Cost: ¥1,700,000、Indirect Cost: ¥510,000)
Fiscal Year 2012: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
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| Outline of Final Research Achievements |
The function of von Willebrand factor (VWF) is essential for normal hemostasis and regulated by ADAMTS13 which cleaves VWF to smaller less-active forms.
We recently found that ADAMTS13 plays a role in safeguarding the myocardium from coronary artery ischemia by reducing VWF-dependent inflammation as well as thrombosis. Next we studied VWF contribution to pathophysiology of sepsis using a mouse model of experimental sepsis involving cecal ligation and puncture (CLP). VWF gene-deleted (VWF-/-; knock-out: KO) mice showed a significantly lower survival rate than wild-type mice after CLP. From those findings, in different types of inflammation, suppression of VWF function may lead to harm body. We need to study more about these differences.
The ratio of VWF-propeptide to ADAMTS13 is associated with disease severity in patients with severe sepsis or septic shock. It means that it may be possible that correcting the imbalance between VWF and ADAMTS13 could be therapeutically useful.
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