Analysis of inframmatory chain mechanism at the wound site through C type lectin receptor (Mincle)

2017 Fiscal Year Final Research Report

• Project/Area Number: 16K15744
• Research Category: Grant-in-Aid for Challenging Exploratory Research
• Allocation Type: Multi-year Fund
• Research Field: Plastic surgery
• Research Institution: Tohoku University
• Principal Investigator: Kei Yoshikawa 東北大学, 医学系研究科, 非常勤講師 (20770978)
• Co-Investigator(Kenkyū-buntansha): 菅野 恵美 東北大学, 医学系研究科, 講師 (10431595) ; 丹野 寛大 東北大学, 医学系研究科, 助教 (10755664) ; 館 正弘 東北大学, 医学系研究科, 教授 (50312004)
• Co-Investigator(Renkei-kenkyūsha): KAWAKAMI Kazuyoshi 東北大学, 医学系研究科, 教授 (10253973)
• Project Period (FY): 2016-04-01 – 2018-03-31
• Keywords: C型レクチン受容体 / 創傷治癒 / 炎症反応

Outline of Final Research Achievements

Macrophage inducible C-type lectin (Mincle) is an activating receptor, expressed in macrophages and dendritic cells, which senses PAMPs and DAMPs. However, the role of Mincle at the wound sites has not been elucidated. In the present study, we addressed a question how defect of Mincle affected to the healing process of wounds.
Wounds were created on the backs of wild type (WT) C57BL/6 and Mincle-deficient (KO) mice. We analyzed percent wound closure, height of granulation tissue, expression of Mincle by real-time PCR and immunohistochemistry.
The percent wound closure was significantly increased in Mincle KO mice compared to WT mice, which was associated with the increased height of granulation tissues. Mincle was detected at the early phase after wound creation. These results suggest that Mincle may be involved in the regulation of granulation at the wounded tissues, which may lead to delayed wound healing.

Free Research Field

形成外科学