Project/Area Number |
26670769
|
Research Category |
Grant-in-Aid for Challenging Exploratory Research
|
Allocation Type | Multi-year Fund |
Research Field |
Plastic surgery
|
Research Institution | Tohoku University |
Principal Investigator |
Usuba Chie 東北大学, 医学(系)研究科(研究院), 非常勤講師 (80509232)
|
Co-Investigator(Kenkyū-buntansha) |
TACHI Masahiro 東北大学, 医学系研究科, 教授 (50312004)
KANNO Emi 東北大学, 医学系研究科, 講師 (10431595)
|
Co-Investigator(Renkei-kenkyūsha) |
KAWAKAMI Kazuyoshi 東北大学, 医学系研究科, 教授 (10253973)
|
Project Period (FY) |
2014-04-01 – 2016-03-31
|
Project Status |
Completed (Fiscal Year 2015)
|
Budget Amount *help |
¥3,770,000 (Direct Cost: ¥2,900,000、Indirect Cost: ¥870,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
Fiscal Year 2014: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
Keywords | 創傷治癒 / 炎症 / C型レクチン受容体 / DAMPs / DAMPs / 創傷治癒学 / ダメージ関連分子パターン(DAMPs) |
Outline of Final Research Achievements |
We addressed the possible involvement of C-type lectin receptors (CLRs) in the wound site. The expression of CLRs (Mincle, Dectin-1, Dectin-2) mRNA in the wounded skin were increased after wound creation. We analyzed the role of caspase recruitment domain-containing protein 9 (CARD9), which is an essential signaling adaptor molecule in NF-κB activation upon triggered through CLRs. The percent wound closure, accumulation of leukocytes, mRNA expression of TNF-α were decreased in CARD9 KO mice. These results suggest that CLRs may involved in the inflammatory response at the wound site.
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