Department of Life Science, Institute of Environmental Medicine, Dongguk University Biomedi Campus, 32, Dongguk-ro, Ilsandong-gu, Goyang-si, Gyeonggi-do, 10326, Republic of Korea.
Bioscience Research Institute, Amorepacific Corporation R&D Center, 1920, Yonggu-daero, Giheung-gu, Yongin-si, Gyeonggi-do, 17074, Republic of Korea.
J Dermatol Sci. 2019 May;94(2):276-283. doi: 10.1016/j.jdermsci.2019.03.003. Epub 2019 Mar 23.
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.
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.
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.
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.
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.
紫外线 B（UVB）辐射是皮肤光损伤的主要原因，包括与光皮肤病、衰老和癌症相关的损伤。尽管许多研究表明红光对皮肤具有光保护作用，但这些作用的机制仍知之甚少。
本研究旨在采用转录组学方法，确定可见光红光对正常人体皮肤成纤维细胞中 UVB 诱导的皮肤损伤的光保护作用。
采用基于下一代测序的转录组分析技术，对转录组变化进行分析，并确定可见光红光和 UVB 暴露差异表达的基因。为了了解鉴定基因之间的生物学网络，进行了基于文献的生物学途径分析。采用定量实时聚合酶链反应（PCR）检测用于选择关键基因的 mRNA 水平验证。
我们观察到可见光红光通过调节基因表达来促进对氧化还原和炎症平衡的适应性反应，以及上调参与 DNA 切除修复过程的基因，从而有助于皮肤细胞对 UVB 的保护。我们还发现，红光诱导的生物学网络中的几个关键基因的表达受到差异调控。
可见光红光通过参与细胞保护过程的基因的转录组调节增强了正常人体皮肤细胞对 UVB 的保护作用。我们从这项下一代测序分析中获得的发现可能有助于更好地理解可见光红光的细胞保护作用，并为进一步的分子或机制研究提供方向。
