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2015 Fiscal Year Final Research Report

Involvement of DAMPs in the inflammatory response at the chronic wound site and the establishment of effective care

Research Project

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Project/Area Number 25463284
Research Category

Grant-in-Aid for Scientific Research (C)

Allocation TypeMulti-year Fund
Section一般
Research Field Fundamental nursing
Research InstitutionTohoku University

Principal Investigator

Kanno Emi  東北大学, 医学(系)研究科(研究院), 講師 (10431595)

Co-Investigator(Kenkyū-buntansha) TACHI Masahiro  東北大学, 医学系研究科, 教授 (50312004)
MARUYAMA Ryoko  東北大学, 医学系研究科, 教授 (10275498)
Co-Investigator(Renkei-kenkyūsha) KAWAKAMI Kazuyoshi  東北大学, 医学系研究科, 教授 (10253973)
Project Period (FY) 2013-04-01 – 2016-03-31
Keywords創傷治癒 / 炎症 / DAMPs
Outline of Final Research Achievements

We addressed the possible involvement of damage-associated molecular patterns (DAMPs) and C-type lectin receptors (CLRs)in the wound site. 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. Next, we analyzed the expression of SAP130 and Mincle in the wound site. Wounds were created on the backs of wild-type and CARD9 gene-disrupted (knockout) mice. We analyzed percent wound closure, accumulation of leukocytes, mRNA expression of cytokines and chemokines by real-time PCR. CARD9 KO mice were exhibited significant attenuation in wound closure compared with WT mice, which was associated with the decreased expression of TNF-α, MIP-1α and MIP-1β mRNA.In an immunohistochemical analysis using WT mice, expression of SAP130 and Mincle were detected in the leukocytes. These results suggest that DAMPs may be involved in the inflammatory response.

Free Research Field

創傷治癒

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Published: 2017-05-10  

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