2013 Fiscal Year Final Research Report
Activation of PPARalpha abrogates the vicious cycle between cutaneous barrier dysfunction and allergic inflammation
| Project/Area Number |
23591649
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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 |
Dermatology
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| Research Institution | Oita University |
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Principal Investigator |
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| Project Period (FY) |
2011 – 2013
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| Keywords | PPARalpha / アトピー性皮膚炎 |
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| 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.
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