| Project/Area Number |
15K15648
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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 |
Plastic surgery
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| Research Institution | Tohoku University |
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Principal Investigator |
Takayuki Aizawa 東北大学, 医学系研究科, 非常勤講師 (00747107)
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| Co-Investigator(Kenkyū-buntansha) |
菅野 恵美 東北大学, 医学系研究科, 講師 (10431595)
館 正弘 東北大学, 医学系研究科, 教授 (50312004)
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| Co-Investigator(Renkei-kenkyūsha) |
KAWAKAMI Kazuyoshi 東北大学, 医学系研究科, 教授 (10253973)
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| Project Period (FY) |
2015-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥3,510,000 (Direct Cost: ¥2,700,000、Indirect Cost: ¥810,000)
Fiscal Year 2016: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2015: ¥1,820,000 (Direct Cost: ¥1,400,000、Indirect Cost: ¥420,000)
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| Keywords | 創傷治癒 / Type I インターフェロン / 創傷治癒学 / Type Ⅰインターフェロン |
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| Outline of Final Research Achievements |
Type I interferons (IFNs) are secreted by many cells upon stimulation via pattern recognition receptors like TLR3 and TLR7, and deliver the activation signal through a specific cell surface IFN-α/β receptor (IFNAR) that consists of IFNAR1 and IFNAR2 chains. Although type I IFNs are well known in their antiviral activity, limited information is available in their role during wound healing. In the present study, we analyzed how defect of IFNAR-mediated signaling affected the wound healing . Wounds were created on the backs of C57BL/6 mice, we examinesd the percent wound closure and accumulation of leukocytes were compared between IFNAR1 gene-disrupted (KO) mice and wild type mice. The percent wound closure was significantly delyed in IFNAR1KO mice compared to WT mice on day 5, which was associated with decreased macrophage accumulation. These results suggest that type I IFNs may be involved in the regulation of the wounds healing.
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