| Project/Area Number |
26461662
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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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| Co-Investigator(Renkei-kenkyūsha) |
KOBAYASHI Takashi 大分大学, 医学部, 教授 (30380520)
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| Project Period (FY) |
2014-04-01 – 2017-03-31
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| Project Status |
Completed (Fiscal Year 2016)
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| Budget Amount *help |
¥4,940,000 (Direct Cost: ¥3,800,000、Indirect Cost: ¥1,140,000)
Fiscal Year 2016: ¥1,300,000 (Direct Cost: ¥1,000,000、Indirect Cost: ¥300,000)
Fiscal Year 2015: ¥1,560,000 (Direct Cost: ¥1,200,000、Indirect Cost: ¥360,000)
Fiscal Year 2014: ¥2,080,000 (Direct Cost: ¥1,600,000、Indirect Cost: ¥480,000)
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| Keywords | アトピー性皮膚炎 / PPARα / 皮膚バリア機能 / アレルギー性炎症 / PPAR / 表皮角化細胞 / フィラグリン / TARC / RANTES / 皮膚炎症 |
|---|
| Outline of Final Research Achievements |
A synthetic ligand for PPARα,Wy14643, downregulated the expressions of TARC and RANTES, which were important chemokines in allergic inflammation of atopic dermatitis (AD), upregulated those of filaggrin, an important epidermal differentiation-related molecule, and upregulated those of anti-microbial peptides, LL-37 and HBD3. On the other hands, PPARβ/δ and PPARγ ligands, GW0742 and ciglitazone, respectively, downregulated the expressions of filaggrin, while they downregulated those of TARC and RANTES and upregulated those of LL-37 and HBD3 as in the case of PPARα ligand. These results suggest that downregulation of PPARα in AD is directly involved in both allergic inflammation and cutaneous barrier dysfunction in the pathogenesis of AD and, thereby, could be a therapeutic target accounting for both aspects.
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