| Autor: |
Júlia T. Oliveira, Vanja Dakic, Gabriela Vitória, Carolina da S.G. Pedrosa, Mayara Mendes, Luiz Guilherme H.S. Aragão, Thyago R. Cardim-Pires, Damien Lelièvre, Daniel Rodrigues Furtado, Roberta O. Pinheiro, Débora Foguel, Lionel Breton, Charbel Bouez, Rodrigo De Vecchi, Marília Zaluar P. Guimarães, Stevens Rehen |
| Rok vydání: |
2022 |
| Předmět: |
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| Zdroj: |
Neurobiology of Aging. 113:108-117 |
| ISSN: |
0197-4580 |
| DOI: |
10.1016/j.neurobiolaging.2022.02.010 |
| Popis: |
Aged and photoaged skin exhibit fine wrinkles that are signs of epidermal inflammation and degeneration. It has been shown that healthy elderly skin expresses amyloidogenic proteins, including α-Synuclein, which are known to oligomerize and trigger inflammation and neurodegeneration. However, little is known about their putative role in skin physiology and sensitivity. To unravel this possible role, we investigated the impact of oligomeric α-Synuclein (Oα-Syn) in 2D and 3D keratinocyte human models. Exogenous Oα-Syn caused degeneration of reconstructed human epidermis (RHE) by diminishing proliferation and thickness of the stratum basale. Oα-Syn also increased NF-kB nuclear translocation in keratinocytes and triggered inflammation in the RHE, by increasing expression of interleukin-1β and tumor necrosis factor-alpha, and the release of tumor necrosis factor-alpha in a time-dependent manner. Dexamethasone and an IL-1β inhibitor partially diminished RHE degeneration caused by Oα-Syn. These findings suggest that Oα-Syn induces epidermal inflammation and decreases keratinocyte proliferation, and therefore might contribute to epidermal degeneration observed in human skin aging. |
| Databáze: |
OpenAIRE |
| Externí odkaz: |
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Full Text from ScienceDirect