2017 Fiscal Year Final Research Report
Study on molecular mechanisms underlying the promotion of wound repair by vitamin E
| Project/Area Number |
15K00816
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| Research Category |
Grant-in-Aid for Scientific Research (C)
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| Allocation Type | Multi-year Fund |
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| Section | 一般 |
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| Research Field |
Eating habits
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| Research Institution | Tottori University |
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Principal Investigator |
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| Co-Investigator(Renkei-kenkyūsha) |
HORIKOSHI YOSUKE 鳥取大学, 医学部, 助教 (60448678)
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| Project Period (FY) |
2015-04-01 – 2018-03-31
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| Keywords | ビタミンE / 創傷治癒 / 細胞極性 / 非抗酸化作用 / PI3キナーゼ / aPKC / Par3 |
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| Outline of Final Research Achievements |
In the present study, we examined whether vitamin E affects wound-mediated HaCaT keratinocyte polarization process including the recruitment of Par3 and aPKC, leading to wound repair independently of its antioxidant activity. Functional assays showed that vitamin E but not other antioxidants enhanced wound closure as well as cell polarization, and regulated the localization and complex formation of Par3 and aPKC in HaCaT cells after wounding. Knockdown of aPKC or Par3 abrogated vitamin E-mediated promotion of the wound closure and cell polarization in HaCaT cells. We also found that aPKC kinase activity was significantly increased in vitamin E-treated cells through activation of phosphatidylinositol 3-kinase (PI3K)/Akt signaling pathway.
Our study has demonstrated that vitamin E promotes the cell polarization and migration in human keratinocytes HaCaT cells after wounding via PI3K/aPKC signaling cascade, resulting in acceleration of wound repair.
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| Free Research Field |
生化学、医科栄養学、酸化ストレス学
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