RNAseq of human buttock skin from healthy controls exposed to solar simulated radiation
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ABSTRACT:
PROVIDER: PRJEB56353 | ENA |
REPOSITORIES: ENA
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Project description:The aim of this study was to investigate cutaneous cellular and molecular events in the photodermatoses (including solar urticaria and photoaggravated atopic dermatitis) following solar simulated ultraviolet radiation (SSR) exposure, and this dataset comprised the healthy controls (HC). Cutaneous biopsies were taken from unexposed skin and from skin exposed to a single low (physiological) dose of SSR, at 30 minutes, 3 hours, 24 hours and 72 hours post-exposure, in n=6 HC. Biopsies were assessed by immunohistochemistry (n=6 HC) and RNA-sequencing analysis (n=4 HC).
2024-03-18 | E-MTAB-12218 | biostudies-arrayexpress
Project description:Despite widespread use of sunscreens that minimize erythema by blocking ultraviolet B (UVB) radiation, incidence rates of melanoma continue to rise. In considering this disparity between intervention and disease prevalence, we investigated the in vivo transcriptome of human skin treated with sunscreen and solar-simulated radiation (ssR). A focal skin area of healthy participants was exposed to ssR at 1 minimal erythema dose (MED), 0.1 MED or 100 J/m2 with or without prior application of sunscreen, or to non-UVB-spectrum of ssR (solar-simulated UVA/visible/infrared radiation: ssA). Skin biopsies were analyzed using expression microarrays.
2011-10-19 | GSE22083 | GEO
Project description:Despite widespread use of sunscreens that minimize erythema by blocking ultraviolet B (UVB) radiation, incidence rates of melanoma continue to rise. In considering this disparity between intervention and disease prevalence, we investigated the in vivo transcriptome of human skin treated with sunscreen and solar-simulated radiation (ssR). A focal skin area of healthy participants was exposed to ssR at 1 minimal erythema dose (MED), 0.1 MED or 100 J/m2 with or without prior application of sunscreen, or to non-UVB-spectrum of ssR (solar-simulated UVA/visible/infrared radiation: ssA). Skin biopsies were analyzed using expression microarrays. Ninety-eight microarrays from 14 healthy human volunteers were analyzed. Focal skin areas of all 14 volunteers were exposed to 0 J/m2, 100 J/m2, 1 minimal erythema dose (MED), and 0.1 MED of solar-simulated radiation (ssR). Eight of the 14 volunteers (Group 1) were also exposed to ssA (ssR minus UVB) that were generated by removing UVB from 0 J/m2, 100 J/m2, 1 minimal erythema dose (MED), and 0.1 MED of ssR. Additionally, 6 of the 14 volunteers (Group 2) were treated with sunscreen of sun protection factor (SPF) 15, and exposed to 0 J/m2, 100 J/m2, 1 minimal erythema dose (MED), and 0.1 MED of ssR. Biopsy was taken 24 hours after exposure from each focal skin area for RNA extraction.
2011-10-18 | E-GEOD-22083 | biostudies-arrayexpress
Project description:Solar urticaria (SU) is clinically characterised by rapid onset sunlight-induced urticaria, but its cutaneous pathophysiology is not well understood. The aim of this study was to investigate cutaneous cellular and molecular events in the evolution of SU responses following solar simulated ultraviolet radiation (SSR) exposure, and compare with responses in healthy controls (HC). Cutaneous biopsies were taken from unexposed skin and from skin exposed to a single low (physiological) dose of SSR, at 30 minutes, 3 hours and 24 hours post-exposure, in n=6 SU patients and n=6 HC. Biopsies were assessed by immunohistochemistry (n=6 SU, n=6 HC) and RNA-sequencing analysis (n=4 SU, n=4 HC). This dataset contains RNAseq data from the SU patients.
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Project description:RNAseq of human buttock skin from patients with solar urticaria exposed to solar simulated radiation
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Project description:Kertinocyte cultures grown in 60 mm petri dishes were placed 186 mm from the solar simulator source (Solar-simulated ultraviolet radiation 1600W Xenon short arc lamp with an Oriel Air Mass 1 Direct Filter, (AM1:D:B; model 81074) and KG2 Short Pass Filter. irradiance 9.84 mW/cm² for UVA (98.3%), 0.174 mW/cm² for UVB (1.7%) and 10 mW/cm² (0.017 mW/cm² erythemally-weighted) for the total UVR irradiance) and received a dose of either 0, 10, 20 and 150 kJ/m2 of unweighted ultraviolet radiation and 0, 10 and 150 kJ/m2 of unweighted ultraviolet radiation with SPF 15 sunscreen filtration (Homosalate 3%, Octisalate 4%, Avobenzone 2%, Titanium dioxide 0.66%) (2 mg/cm2 sandwiched between two 5x5 inch quartz plates) and were temperature controlled at 37oC using a customized water-bath. Six and Twenty-four hours post-exposure cells were harvested and RNA was extracted and subjected to microarray analysis.
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Project description:Ultraviolet radiation (UVR) from sunlight is the major effector for skin aging and carcinogenesis. However, genes and pathways altered by solar-simulated UVR (ssUVR), a mixture of UVA and UVB, are not well characterized. Here we report global changes in gene expression as well as associated pathways and upstream transcription factors in human keratinocytes exposed to ssUVR. Human HaCaT keratinocytes were exposed to either a single dose or 5 repetitive doses of ssUVR. Comprehensive analyses of gene expression profiles as well as functional annotation were performed at 24 hours post irradiation. Our results revealed that ssUVR modulated genes with diverse cellular functions in a dose-dependent manner. Gene expression in cells exposed to a single dose of ssUVR differed significantly from those that underwent repetitive exposures. While single ssUVR caused a significant inhibition in genes involved in cell cycle progression, especially G2/M checkpoint and mitotic regulation, repetitive ssUVR lead to extensive changes in genes related to cell signaling and metabolism. We have also identified a panel of ssUVR target genes that exhibited persistent changes in gene expression even at 1 week after irradiation. These results revealed a complex network of transcriptional regulators and pathways that orchestrate the cellular response to ssUVR.
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Project description:Carbaryl (1-naphthyl-methylcarbamate), a broad-spectrum insecticide, has recently been associated with the development of cutaneous melanoma in an epidemiological cohort study with U.S. farm workers also exposed to ultraviolet radiation, which is known to be the main etiologic factor for skin carcinogenesis. Although comprehensive and well designed, the agricultural epidemiological study was not sufficient to characterize the direct contribution of the insecticide and solar radiation in melanomagenesis. Several studies have explored the synergistic effect of certain chemicals with UV radiation, increasing its deleterious effects on the skin. We hypothesized that carbaryl exposure associated with UV solar radiation may induce melanocyte transformation. This study aimed to characterize human melanocytes after individual or combined exposure to carbaryl (100 μM) and solar radiation (375 mJ/cm2). In a microarray analysis, carbaryl, but not solar radiation, induced an important oxidative stress response, evidenced by the upregulation of antioxidant genes, such as Hemeoxygenase-1 (HMOX1), and downregulation of Microphtalmia-associated Transcription Factor (MITF), the main regulator of melanocytic activity; results were confirmed by qRT-PCR. Carbaryl and solar radiation induced a gene response suggestive of DNA damage and cell cycle alteration. The expression of genes in these categories was notably more intense in the combined treatment group, in a synergistic manner, for CDKN1A, BRCA1/2 and MDM2 genes. Likewise, flow cytometry assays demonstrated S-phase cell cycle arrest, reduced apoptosis levels and faster induction of cyclobutane pyrimidine dimers (CPD) lesions in carbaryl treated groups. Our data suggests that carbaryl is genotoxic to human melanocytes, especially when associated with solar radiation.
2017-03-15 | GSE79579 | GEO
Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system.
2014-08-27 | GSE60795 | GEO
Project description:Skin damage from solar ultraviolet radiation (UVR) accumulates in the dermal extracellular matrix (ECM) and contributes to photoaging. Following UVR exposure, matrix metalloproteinases (MMPs) are secreted by dermal fibroblasts to repair and remodel the ECM. Molecular signaling pathways delineating the induction of MMPs are currently well-defined; however, the effects of UV exposure on epigenetic mechanisms of MMP induction are not as well understood. An epigenetic mechanism would further describe how MMP genes are regulated in response to UV. In this study, we examined solar simulated UVR (ssUVR)-induced gene expression changes and alterations to histone methylation in the promoters of MMP1 and MMP3 in primary human dermal fibroblasts (HDF). This set of gene expression data was generated to identify photoaging related genes (including MMP) that were impacted by ssUVR exposure in our system.
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