Abstract
Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin. It was revealed that chronic exposure to UVR accelerates skin aging, induces immunosuppression and may lead to the development of skin cancers. On the other hand, UVR has been shown to be effective in the treatment of numerous skin diseases and thus, various phototherapy modalities have been developed to date. Narrow-band ultraviolet B (NB-UVB) emitting a light with a peak around 311 nm has been demonstrated to be effective in the treatment of various skin disorders; currently it is one of the most commonly used phototherapy devices. Despite NB-UVB has been developed more than 30 years ago, the exact mechanism of its therapeutic action remains poorly understood. To date, most of NB-UVB effects were attributed to its influence on immune cells; however, nearly 90% of NB-UVB irradiation is absorbed by epidermis and keratinocytes seem to be important players in mediating NB-UVB biological activity. Here, we have reviewed the current data about the influence of NB-UVB on epidermal cells, with a special emphasis on cell proliferation and death.
Highlights
Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin
Narrow-band ultraviolet B (NB-UVB) altered the lipidome of keratinocytes in a pattern of changes consisting with unfolding apoptosis. Whether these observations have clinical relevance, one may speculate that increased synthesis of ceramides and TAGs after NB-UVB irradiation in apoptosis-undergoing cells may help in restoration of abnormal epidermal lipid composition in patients suffering from atopic dermatitis or psoriasis, an idea which has been already suggested by Wefers et al [53]
NB-UVB is able to inhibit cell proliferation as well as is able to induce apoptosis of various cell types. This action may be responsible for its therapeutic activity in diseases with a high proliferation rate, such as psoriasis
Summary
Ultraviolet radiation (UVR) is known to be one of the most important environmental hazards acting on the skin. Several studies have shown that NB-UVB inhibits proliferation and is able to induce apoptosis in human keratinocytes, both in vitro and in vivo [19,20,21,22,23,24,25]. Repeated NB-UVB exposures decreased the level of survivin (an anti-apoptotic protein) in psoriatic epidermis in vivo, enabling epidermal cells to undergo apoptosis [31].
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