Effects of UVB-induced oxidative stress on protein expression and specific protein oxidation in normal human epithelial keratinocytes: a proteomic approach

The expression levels of fifteen proteins - involved in maintaining the cytoskeleton integrity, removal of damaged proteins and heat shock response - were differentially regulated in UVB-exposed cells, indicating that an appropriate response is developed in order to counteract/neutralize the toxic effects of UVB-raised ROS. On the other side, the redox proteomics approach revealed that seven proteins - involved in cellular adhesion, cell-cell interaction and protein folding - were selectively oxidized.Despite a wide and well orchestrated cellular response, a relevant oxidation of specific proteins concomitantly occurs in UVB-irradiated human epithelial Keratinocytes. These modified (i.e. likely dysfunctional) proteins might result in cell homeostasis impairment and therefore eventually promote cellular degeneration, senescence or carcinogenesis.The skin is the largest organ of the human body. It provides a major anatomical barrier between the internal and external environment. The body is constantly exposed to an array of chemical and physical exogenous pollutants. The outermost layer of the skin is composed predominantly by keratinocytes that provide a barrier between the host and the environment. Keratinocytes are continuously exposed to UV irradiation, which is able to induce a dramatic surge of biological events such as sunburn, inflammation, cellular/tissue injury, cell death, and skin cancer. Although UVB (290-320 nm) represents only 4% of the total solar UV radiation, it is responsible for the development of skin cancer in humans such as melanoma as well as non melanoma skin cancer [1].Increasing evidence indicates that the UVB response in the skin is a complex and multifaceted biological process. The UVB signal transduction originates at multiple intracellular sites and the cross talk between dedicated molecular mediators acting within a complex signal network determines the fate of a UVB damaged cell. Even if very little is known about the original signalli