Activation of PPARalpha abrogates the vicious cycle between cutaneous barrier dysfunction and allergic inflammation
Project/Area Number |
23591649
|
Research Category |
Grant-in-Aid for Scientific Research (C)
|
Allocation Type | Multi-year Fund |
Section | 一般 |
Research Field |
Dermatology
|
Research Institution | Oita University |
Principal Investigator |
|
Project Period (FY) |
2011 – 2013
|
Project Status |
Completed (Fiscal Year 2013)
|
Budget Amount *help |
¥5,200,000 (Direct Cost: ¥4,000,000、Indirect Cost: ¥1,200,000)
Fiscal Year 2013: ¥1,170,000 (Direct Cost: ¥900,000、Indirect Cost: ¥270,000)
Fiscal Year 2012: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2011: ¥2,470,000 (Direct Cost: ¥1,900,000、Indirect Cost: ¥570,000)
|
Keywords | PPARalpha / アトピー性皮膚炎 / PPARα / 皮膚バリア機能 / アレルギー性炎症 / 表皮角化細胞 / ケモカイン |
Research Abstract |
Expressions of TARC and RANTES in epidermal keratinocytes, which are important chemokines in the pathogenes of atopic dermatitis (AD), were up-regulated by knockdown of PPARalpha. On the other hands, expressions of loricrin and transglutaminase 1, which are important epidermal differentiation-related molecules, were down-regulated in PPARalpha-knockdown epidermal keratinocytes. In addition, a PPARalpha agonist down-regulated the expressions of TARC and RANTES and up-regulated those of filaggrin, which is known to be decreased in AD, respectively in epidermal keratinocytes. These results suggest not only that reduction of PPARalpha is involved in both of cutaneous barrier abnormalities and allergic inflammation in the pathogenesis of AD but also that activation of PPARalpha might be a new therapeutic strategy which targets the both aspects in AD.
|
Report
(4 results)
Research Products
(13 results)