Abstract:
BACKGROUND:Ultraviolet B (UVB) radiation is a major cause of skin photodamage, including the damage associated with photodermatoses, aging, and cancer. Although many studies have shown that red light has photoprotective effects on skin, the mechanisms underlying these effects are still poorly understood. OBJECTIVE:The aim of this study was to identify the photoprotective effects of visible red light against UVB-induced skin damage in normal human dermal fibroblast cells using a transcriptomic approach. METHODS:Next-generation sequencing-based transcriptomic analyses were used to profile transcriptomic alterations and identify genes that are differentially expressed by visible red light and by UVB exposure. To understand the biological networks among identified genes, a literature-based biological pathway analysis was performed. Quantitative real-time polymerase chain reaction assays were used for mRNA-level validation of selected key genes. RESULTS:We observed that visible red light contributes to skin cell protection against UVB by modulating gene expression that enhances the adaptive response to redox and inflammatory balancing and by upregulating genes involved in DNA excision repair processes. We also identified that several key genes in the red light-induced biological network were differentially regulated. CONCLUSIONS:Visible red light enhanced the UVB-protective effects in normal human skin cells via the transcriptomic modulation of genes involved in cell-protective processes. Our findings from this next-generation sequencing analysis may lead to a better understanding of the cytoprotective effects of visible red light and provide direction for further molecular or mechanistic studies.
journal_name
J Dermatol Scijournal_title
Journal of dermatological scienceauthors
Kim HS,Kim YJ,Kim SJ,Kang DS,Lee TR,Shin DW,Kim HJ,Seo YRdoi
10.1016/j.jdermsci.2019.03.003subject
Has Abstractpub_date
2019-05-01 00:00:00pages
276-283issue
2eissn
0923-1811issn
1873-569Xpii
S0923-1811(19)30068-4journal_volume
94pub_type
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