Neuronal and non-neuronal transient receptor potential ankyrin 1 mediates UVB radiation-induced skin inflammation in mice.

AIMS:Neuronal and non-neuronal TRPA1 channel plays an active role in the pathogenesis of several skin inflammatory diseases. Although a recent study identified the TRPA1 channel activation upon UVB exposure, its role in inflammatory, oxidative, and proliferative processes underlying UVB radiation-induced sunburn was not yet fully understood. We evaluated the TRPA1 channel contribution in inflammatory, oxidative, and proliferative states on skin inflammation induced by UVB radiation in mice. MAIN METHODS:TRPA1 role was evaluated from inflammatory (ear edema, myeloperoxidase, and N-acetyl-β-D-glycosaminidase activities, histological changes, and cytokines levels), proliferative (epidermal hyperplasia, PCNA, and TRPA1 levels), and oxidative (reactive oxygen intermediates measure, H₂O₂ quantification, and NADPH oxidase activity) parameters caused by UVB radiation single (0.5 J/cm²) or repeated (0.1 J/cm²) exposure. We verified the contribution of non-neuronal and neuronal TRPA1 on UVB radiation-induced inflammatory parameters using RTX-denervation (50 μg/kg s.c.). KEY FINDINGS:TRPA1 blockade by the selective antagonist Lanette® N HC-030031 reduced all parameters induced by UVB radiation single (at concentration of 1%) or repeated (at concentration of 0.1%) exposure. We evidenced an up-regulation of the TRPA1 protein after UVB radiation repeated exposure, which was blocked by topical Lanette® N HC-030031 (0.1%). By RTX-denervation, we verified that non-neuronal TRPA1 also interferes in some inflammatory parameters induction. However, cutaneous nerve fibers seem to be most needed in the development of UVB radiation-induced inflammatory processes. SIGNIFICANCE:We propose the TRPA1 channel participates in the UVB radiation-induced sunburn in mice, and it could be a promising therapeutic target to treat skin inflammatory disorders.

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