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OLIGOMERIC α-SYNUCLEIN INDUCES SKIN DEGENERATION IN RECONSTRUCTED HUMAN EPIDERMIS
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Abstract
Aged and photoaged skin exhibit fine wrinkles that are signs of epidermal inflammation and degenera- tion. 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 inves- tigated the impact of oligomeric α-Synuclein (O α-Syn) in 2D and 3D keratinocyte human models. Exoge- nous O α-Syn caused degeneration of reconstructed human epidermis (RHE) by diminishing proliferation and thickness of the stratum basale. O α-Syn also increased NF-kB nuclear translocation in keratinocytes and triggered inflammation in the RHE, by increasing expression of interleukin-1 βand tumor necrosis factor-alpha, and the release of tumor necrosis factor-alpha in a time-dependent manner. Dexamethasone and an IL-1 βinhibitor partially diminished RHE degeneration caused by O α-Syn. These findings sug- gest that O α-Syn induces epidermal inflammation and decreases keratinocyte proliferation, and therefore might contribute to epidermal degeneration observed in human skin aging.
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