| Project/Area Number |
23659491
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| Research Category |
Grant-in-Aid for Challenging Exploratory Research
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| Allocation Type | Multi-year Fund |
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| Research Field |
Hematology
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| Research Institution | Kagoshima University |
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Principal Investigator |
MARUYAMA Ikuro 鹿児島大学, 医歯学総合研究科, 特任教授 (20082282)
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| Co-Investigator(Kenkyū-buntansha) |
KAWAHARA Koichi 大阪工業大学, 工学部, 教授 (10381170)
HASHIGUCHI Teruto 鹿児島大学, 大学院・医歯総合研究科, 教授 (70250917)
OYAMA Yoko 鹿児島大学, 医学部・歯学部附属病院, 特任助教 (20583470)
ITO Takashi 鹿児島大学, 大学院・医歯総合研究科, 特任講師 (20381171)
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| Project Period (FY) |
2011
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| Project Status |
Completed (Fiscal Year 2011)
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| Budget Amount *help |
¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
Fiscal Year 2011: ¥3,900,000 (Direct Cost: ¥3,000,000、Indirect Cost: ¥900,000)
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| Keywords | 血栓 / 止血学 / トロンボモジュリン / トロンビン / HMGB1 / DIC / des-HMGB1 |
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| Research Abstract |
We previously showed that HMGB1 binds to thrombomodulin(TM) and degraded by thrombin-TM at the N-terminus of the molecule cleaving out 10 aminoacdid-residue. We named this degraded HMGB1 as des-HMGB1. We also have showed that des-HMGB1 compete with intact binding to its receptor RAGE, Toll-like receptor-2 and-4 resulting negatively regulating of intact HMGB1 and its receptor signaling.
In this study, we established the des-HMGB1 specific assay ELISA, and investigated its dynamism in various diseases including DIC, sepsis and shock. We showed that the des-HMGB1 was increased in the serum from the patients with these pathologic conditions, especially in the cases treated with recombinant TM. We are now further studying relationship between des-HMGB1 levels and the efficacy of TM treatment and their prognosis.
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