Issue 1, 2012

Modulation of gene expression by the oxidative stress generated in human skin cells by UVA radiation and the restoration of redox homeostasis

Abstract

UVA radiation generates a significant oxidative stress in skin cells which is further enhanced by the release of the pro-oxidant catalysts iron and heme, and exacerbated by UVA-mediated destruction of cellular reducing equivalents and the antioxidant enzyme catalase. An important consequence of this altered redox state is the generation of oxidized membrane components in the form of 4-hydroxynonenal, ceramides and oxidized phospholipids, all of which are potent signalling molecules which lead to modulation of the expression of many genes. Transcription factors (such as nuclear factor kappa-light-chain-enhancer of activated B cells) and several genes (e.g. interleukins, intercellular adhesion molecule and 1, hemeoxygenase 1) involved in the inflammatory response are dramatically modified by UVA. Levels of both antioxidant and pro-oxidant proteins, including manganese-dependent superoxide dismutase, glutathione peroxidase, hemeoxygenase 1, NADPH oxidase, ferritin, and methionine-S-sulfoxidereductase, are increased by UVA treatment and following moderate dose levels these will contribute to either the restoration or a further perturbation of redox homeostasis. Finally, UVA induces a whole set of matrix metalloproteinases and proteases, primarily in cells of dermal origin, which can contribute to the long-term consequences of UVA exposure of skin.

Graphical abstract: Modulation of gene expression by the oxidative stress generated in human skin cells by UVA radiation and the restoration of redox homeostasis

Article information

Article type
Perspective
Submitted
14 Jul 2011
Accepted
15 Sep 2011
First published
19 Oct 2011

Photochem. Photobiol. Sci., 2012,11, 135-147

Modulation of gene expression by the oxidative stress generated in human skin cells by UVA radiation and the restoration of redox homeostasis

R. M. Tyrrell, Photochem. Photobiol. Sci., 2012, 11, 135 DOI: 10.1039/C1PP05222E

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