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Distinctive molecular responses to ultraviolet radiation between keratinocytes and melanocytes.

ABSTRACT: Solar ultraviolet radiation (UVR) is the major risk factor for skin carcinogenesis. To gain new insights into the molecular pathways mediating UVR effects in the skin, we performed comprehensive transcriptomic analyses to identify shared and distinctive molecular responses to UVR between human keratinocytes and melanocytes. Keratinocytes and melanocytes were irradiated with varying doses of UVB (10, 20 and 30 mJ/cm(2) ) then analysed by RNA-Seq at different time points post-UVB radiation (4, 24 and 72 h). Under basal conditions, keratinocytes and melanocytes expressed similar number of genes, although they each expressed a distinctive subset of genes pertaining to their specific cellular identity. Upon UVB radiation, keratinocytes displayed a clear pattern of time- and dose-dependent changes in gene expression that was different from melanocytes. The early UVB-responsive gene set (4 h post-UVR) differed significantly from delayed UVB-responsive gene sets (24 and 72 h). We also identified multiple novel UVB signature genes including PRSS23, SERPINH1, LCE3D and CNFN, which were conserved between melanocyte and keratinocyte lines from different individuals. Taken together, our findings elucidated both common and distinctive molecular features between melanocytes and keratinocytes and uncovered novel UVB signature genes that might be utilized to predict UVB photobiological effects on the skin.

SUBMITTER: Sun X

PROVIDER: S-EPMC5295856 | biostudies-literature | 2016 Sep

REPOSITORIES: biostudies-literature

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Distinctive molecular responses to ultraviolet radiation between keratinocytes and melanocytes.

Sun Xiaoyun X Kim Arianna A Nakatani Masashi M Shen Yao Y Liu Liang L

Experimental dermatology 20160630 9

Solar ultraviolet radiation (UVR) is the major risk factor for skin carcinogenesis. To gain new insights into the molecular pathways mediating UVR effects in the skin, we performed comprehensive transcriptomic analyses to identify shared and distinctive molecular responses to UVR between human keratinocytes and melanocytes. Keratinocytes and melanocytes were irradiated with varying doses of UVB (10, 20 and 30 mJ/cm(2) ) then analysed by RNA-Seq at different time points post-UVB radiation (4, 24 ...[more]

PMID: 27119462

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Project description:BackgroundHuman skin, which is constantly exposed to solar ultraviolet radiation (UVR), has a unique ability to respond by increasing its pigmentation in a protective process driven by melanogenesis in human epidermal melanocytes (HEMs). However, the molecular mechanisms used by HEMs to detect and respond to UVR remain unclear.ObjectivesTo investigate the function and potential mechanism of opsin 5 (OPN5), a photoreceptor responsive to UVR wavelengths, in melanogenesis in HEMs.MethodsMelanin content in HEMs was determined using the NaOH method, and activity of tyrosinase (TYR) (a key enzyme in melanin synthesis) was determined by the l-DOPA method. OPN5 expression in UVR-treated vs. untreated HEMs and explant tissues was detected by reverse-transcription quantitative polymerase chain reaction (RT-qPCR), Western blotting and immunofluorescence. Short interfering RNA-mediated OPN5 knockdown and a lentivirus OPN5 overexpression model were used to examine their respective effects on TYR, tyrosinase-related protein 1 (TRP1), TRP2 and microphthalmia-associated transcription factor (MITF) expression, under UVR. Changes in expression of TYR, TRP1 and TRP2 caused by changes in OPN5 expression level were detected by RT-qPCR and Western blot. Furthermore, changes in signalling pathway proteins were assayed.ResultsWe found that OPN5 is the key sensor in HEMs responsible for UVR-induced melanogenesis. OPN5-induced melanogenesis required Ca2+ -dependent G protein-coupled receptor- and protein kinase C signal transduction, thus contributing to the UVR-induced MITF response to mediate downstream cellular effects, and providing evidence of OPN5 function in mammalian phototransduction. Remarkably, OPN5 activation was necessary for UVR-induced increase in cellular melanin and has an inherent function in melanocyte melanogenesis.ConclusionsOur results provide insight into the molecular mechanisms of UVR sensing and phototransduction in melanocytes, and may reveal molecular targets for preventing pigmentation or pigment diseases.

Project description:BackgroundSunburn is the strongest risk factor for melanoma and non-melanoma skin cancers. Adolescent sunburns are related to higher risk of developing melanoma later in life. Little is known about the association of sunburns and shade, particularly tree cover, around adolescent homes and schools. This linkage study assessed associations of adolescent self-reported sunburns with ambient ultraviolet radiation (UV) and tree cover.MethodsWe analyzed a U.S. national sample of parent-child dyads (n?=?1333) from the 2014 Family Life, Activity, Sun, Health, and Eating (FLASHE) study conducted by the National Cancer Institute. The outcome was adolescent sunburns reported for the previous 12 months. GIS buffers around geocoded home and school addresses were used to summarize UV and tree cover. A sensitivity analysis assessed different UV measures and tree cover buffer distances. Logistic regression models estimated the adjusted odds of any sunburns for five models: (1) no environmental variables; (2) spatial variables of latitude and longitude; (3) UV; (4) tree cover; and, (5) a combined model with UV and tree cover. Covariates included common sunburn-related items such as sun protective behaviors, socio-demographics, and latitude. Model residuals were assessed for spatial dependency and clustering.ResultsOverall, 44% of adolescents reported any sunburns in the previous 12 months. For the bivariate associations, lower categories of UV were associated with any reported sunburns (p-trend?=?0.002). Home tree cover was not associated with any reported sunburns (p-trend?=?0.08), whereas schools with lower categories of tree cover were associated with sunburns (p-trend?=?0.008). The adjusted odds of any sunburns by UV tertiles, as a linear tread, was 0.89 (0.76-1.05) (p?=?0.17); school tree cover was: 0.91 (0.78-1.07) (p?=?0.25). Neither UV nor tree cover, in a combined model, were significant. Sensitivity analyses resulted in the optimal buffer size of 200 m for summarizing tree cover. Spatial dependence of residuals was not significant and clustering was significant for about 6% or less of the sample in each model.ConclusionsWe did not find significant relationships between UV or tree cover and adolescent sunburns, when adjusted by sunburn-related covariates. Better contextual data about where sunburns occurred is needed to identify environmental correlates of sunburn.

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Distinctive molecular responses to ultraviolet radiation between keratinocytes and melanocytes.

Publications

Distinctive molecular responses to ultraviolet radiation between keratinocytes and melanocytes.

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