Study on molecular mechanisms underlying the promotion of wound repair by vitamin E
Project/Area Number |
15K00816
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Eating habits
|
Research Institution | Tottori University |
Principal Investigator |
|
Co-Investigator(Renkei-kenkyūsha) |
HORIKOSHI YOSUKE 鳥取大学, 医学部, 助教 (60448678)
|
Project Period (FY) |
2015-04-01 – 2018-03-31
|
Project Status |
Completed (Fiscal Year 2017)
|
Budget Amount *help |
¥4,550,000 (Direct Cost: ¥3,500,000、Indirect Cost: ¥1,050,000)
Fiscal Year 2017: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,950,000 (Direct Cost: ¥1,500,000、Indirect Cost: ¥450,000)
|
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 / エストロゲン受容体 |
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.
|
Report
(4 results)
Research Products
(35 results)
-
-
-
-
-
[Journal Article] Nicotine enhances the malignant potential of human pancreatic cancer cells via activation of atypical protein kinase C.2016
Author(s)
Hanaki T, Horikoshi Y, Nakaso K, Nakasone M, Kitagawa Y, Amisaki M, Arai Y, Tokuyasu N, Sakamoto T, Honjo S, Saito H, Ikeguchi M, Yamashita K, Ohno S and Matsura T
-
Journal Title
Biochim Biophys Acta
Volume: 1860
Issue: 11
Pages: 2404-2415
DOI
Related Report
Peer Reviewed / Open Access / Acknowledgement Compliant
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-
-