Neuronal and non-neuronal transient receptor potential ankyrin 1 mediates UVB radiation-induced skin inflammation in mice
| Autor: | Evelyne da Silva Brum, Camila Camponogara, Eunice André, Margareth de Mello Brandenburg, Indiara Brusco, Gabriela Trevisan, Daniela Almeida Cabrini, Sara Marchesan Oliveira, Natháli Schopf Pegoraro, Fernanda Grillo Rocha |
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| Rok vydání: | 2020 |
| Předmět: |
Male
0301 basic medicine Ultraviolet Rays Resiniferatoxin Inflammation Oxidative phosphorylation Pharmacology medicine.disease_cause 030226 pharmacology & pharmacy General Biochemistry Genetics and Molecular Biology Pathogenesis Mice 03 medical and health sciences Transient receptor potential channel chemistry.chemical_compound 0302 clinical medicine medicine Animals Edema General Pharmacology Toxicology and Pharmaceutics Sunburn skin and connective tissue diseases TRPA1 Cation Channel Peroxidase Skin Neurons integumentary system biology Chemistry food and beverages Hydrogen Peroxide General Medicine medicine.disease Disease Models Animal 030104 developmental biology Myeloperoxidase biology.protein Cytokines medicine.symptom psychological phenomena and processes Oxidative stress |
| Zdroj: | Life Sciences. 262:118557 |
| ISSN: | 0024-3205 |
| DOI: | 10.1016/j.lfs.2020.118557 |
| Popis: | 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. |
| Databáze: | OpenAIRE |
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