| Project/Area Number |
22791089
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| Research Category |
Grant-in-Aid for Young Scientists (B)
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| Allocation Type | Single-year Grants |
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| Research Field |
Dermatology
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| Research Institution | Keio University |
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Principal Investigator |
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| Project Period (FY) |
2010 – 2011
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| Project Status |
Completed (Fiscal Year 2011)
|
| Budget Amount *help |
¥4,030,000 (Direct Cost: ¥3,100,000、Indirect Cost: ¥930,000)
Fiscal Year 2011: ¥1,690,000 (Direct Cost: ¥1,300,000、Indirect Cost: ¥390,000)
Fiscal Year 2010: ¥2,340,000 (Direct Cost: ¥1,800,000、Indirect Cost: ¥540,000)
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| Keywords | 重層扁平上皮 / 可視化 / Tight junction / Tight Junction / 表皮バリア |
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| Research Abstract |
Mammalian skin consists of two sets of barriers : stratum corneum(SC) and tight junctions(TJs). Filaggrin is a structural protein of SC. The loss-of-function mutations in filaggrin gene are reported as a major predisposing factor for atopic dermatitis, suggesting that disrupted SC barrier might result in increased entry of external antigens. Epidermal TJ also functions as an outside-in barrier, however, TJ barrier function under filaggrin-deficient conditions has not been investigated. In this study, we examined the epidermal TJ structure and functions in filaggrin knockout mice, which completely lack filaggrin expression in the epidermis. 3D structure of epidermal TJ was investigated in a whole-mounted ear epidermis using confocal microscopy. In filaggrin KO mice, the expression and localization of TJ-related proteins were not affected. TJ-permeability assay using a primary amine-reactive biotinylation reagent as a tracer revealed that the barrier function of TJ against water-soluble～ 500 dalton molecule was neither altered in neonatal mouse nor adult mice of these filaggrin-deficient models. These results suggested that the absence of filaggrin does not alter the barrier function of TJ directly.
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