Scratch damaged tight junction through Akt/CLDN1 axis in atopic dermatitis.

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Atopic dermatitis (AD) is a common, chronic, severely pruritic, eczematous skin disease that seriously deteriorates the quality of life of patients. Scratch is a cardinal symptom of AD. Although the vicious "itch-scratch cycle" continues and aggravates skin barrier dysfunction in AD, how scratch induces skin barrier dysfunction through tight junction remains unclear.To study the effect of scratch on tight junction in "itch-scratch cycle".Evaluation of itch behavior and skin barrier dysfunction in neck and back AD model were assessed. The expression of tight junction proteins was compared between neck and back models and the mechanisms underlying the involvement of Akt/CLDN1 pathways in this process were explored.we performed oxazolone to induce AD mice model in neck and back, this model generated significantly itch behavior and more pronounced skin barrier dysfunction in neck. The down-regulation of claudin-1 (CLDN1) and up-regulation of Akt phosphorylation in skin were well correlated with scratch behavior in AD model, Furthermore, SC79, the agonist of Akt phosphorylation, which could down-regulated CLDN1 expression in HaCaT cell. Then the antagonist of Akt phosphorylation (LY294002) was used to treat AD mice, which could rescue the expression of CLDN1 through inhibiting the Akt phosphorylation in skin. Importantly, the scratch behavior induced by AD also been inhibited by LY294002 treatment.The results reveal the underlying mechanism of tight junction damage promoted by scratch in the "itch-scratch cycle" of AD, and opened a new avenue to itch management in AD.


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