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KMID : 0984920160180020055
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Journal of Skin Barrier Research
2016 Volume.18 No. 2 p.55 ~ p.56
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Effects of PAR2-Antagonist on Inflammatory Signals and Tight Junction Expression in Protease Activated Canine Primary Epithelial Keratinocytes
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Kim Ha-Jung
Jeong Se-Kyoo
Hong Soo-Jong
Kim Ahrens
Marsella Rosanna
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Abstract
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Atopic dermatitis (AD) is a common allergic eczematous skin disorder in humans, the incidence of which is increasing worldwide. Protease activated receptor 2 (PAR2) is a mediator of innate immunity expressed on keratinocytes that can induce Th2-related inflammation in AD.
Using a validated canine model of spontaneously occurring AD, we previously assessed the expression of PAR2 and thymic stromal lymphopoietin (TSLP) and reported that the expression pattern of skin biopsy samples differed in normal and atopic dogs. Pilot studies in our canine atopic model have also shown decrease tight junction protein expression such as and Zonula Occludens-1 (ZO-1)
This study investigated whether PAR2 mediates the expression of TSLP and ZO-1 in canine primary epithelial keratinocytes (CPEKs) by assessing the effects of a PAR2-antagonist (PAR2-ant) on PAR2, TSLP, and ZO-1 immunofluorescence.
CPEKs were cultured with serine protease over time with or without PAR2-antagonist and the expressions were quantitated by real-time PCR and fluorescence intensity in CPEKs. Protease significantly increased the expressions of PAR2 and TSLP, but decreased the expression of ZO-1 at each specific incubation time. PAR2-antagonist blocked those effects on each mediator and tight junction. Therefore, blockage of PAR2 can suppress the trypsin-activated initiation of inflammatory signals and the disturbance of tight junction protein CPEK.
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