UV irradiation of human melanocytes
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE9016 | GEO | 2007/09/15
SECONDARY ACCESSION(S): PRJNA102507
REPOSITORIES: GEO
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Project description:Target genes of ultraviolet stress response in cutaneous melanocytes, potentially associated with solar induced melanocarcinogenesis, were characterized by cDNA microarray technology. In cultured normal human melanocytes, 198 genes out of »9000 arrayed were found modulated > 1.9 times following artificial ultraviolet (mainly ultraviolet-B) irradiation (100 mJ per cm2).
2007-09-15 | E-GEOD-9016 | biostudies-arrayexpress
Project description:The response of microRNAs (miRNAs) to solar ultraviolet radiation (UVR) in human melanocytes while in their natural environment, and in particular, melanocytes from persons with a history of melanoma versus those from healthy persons, have yet to be described. Here, we used laser capture microdissection (LCM) to isolate and subsequently profile the expression of miRNAs in a pure population of melanocytes from human volunteers exposed to physiological doses of simulated sunlight (ssUVR). The majority of the UV-responsive miRNAs in the melanocytes of melanoma patients were down-regulated in expression when compared to those in the melanocytes of healthy individuals. De-repressed genes associated with these down-regulated UV-miRNAs belonged to regulatory modules involved in controlling the epithelial-to-mesenchymal transition (EMT), apoptosis, and immune-evasion, processes reputedly linked to melanoma.
2016-05-24 | GSE75621 | GEO
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:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target. Biologic replicates of UVA- and UVB-treated mouse melanocytes, as well as untreated mouse melanocytes and mouse keratinocytes, were used to define melanocyte expression signatures associated with UV treatment.
2011-01-01 | E-GEOD-25164 | biostudies-arrayexpress
Project description:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target.
2011-01-01 | GSE25164 | GEO
Project description:We analysed the whole-genome transcriptional profile of 6 cell lines of dark melanocytes (DM) and 6 of light melanocytes (LM) at basal conditions and after UVB at different time points (6, 12 and 24h) to investigate the mechanisms by which melanocytes protect human skin from the damaging effects of ultraviolet-B radiation (UVB). Further, we assessed the effect of different keratinocyte-conditioned media (KCM+ and KCM-) on melanocytes.
2015-08-08 | GSE70280 | GEO
Project description:We analysed the whole-genome transcriptional profile of 6 cell lines of dark melanocytes (DM) and 6 of light melanocytes (LM) at basal conditions and after UVB at different time points (6, 12 and 24h) to investigate the mechanisms by which melanocytes protect human skin from the damaging effects of ultraviolet-B radiation (UVB). Further, we assessed the effect of different keratinocyte-conditioned media (KCM+ and KCM-) on melanocytes. We analysed six lines of melanocytes isolated from lightly pigmented neonatal foreskin (LM), and six lines from darkly pigmented neonatal foreskin (DM), at 0, 6, 12 and 24 hours post UV irradiation. We also assessed the effect of different keratinocyte-conditioned media (KCM+ or KCM-)
2015-08-08 | E-GEOD-70280 | biostudies-arrayexpress
Project description:Ultraviolet radiation (UVR) is the greatest risk factor for melanoma development. While the role of UVR in DNA mutagenesis is generally accepted, the role of UVR-induced mutations in melanomagenesis remains controversial. To understand better how UVR is contributing to melanoma development, we investigated the non-mutational effect of UVR on the epigenome, specifically DNA methylation. Aberrant DNA methylation changes are a hallmark in melanoma and there are few reports on the effects of UVR on DNA methylation. We exposed melanocytes to UVR and cultured them for one-month to detect heritable and stable changes in DNA methylation. We found both hyper and hypo methylated sites after UVR exposure. While many of these changes occurred outside of promoters and areas of active gene expression, there were changes in promoter DNA methylation changes that correlated with changes in gene expression. These changes also correlated with those found in melanoma and UVR sensitive sites were prognostic of patient overall survival. Our work shows UVR-induced DNA methylation changes in melanocytes and may be a novel non-mutational mechanism in which UVR contributes to melanoma development.
2024-03-25 | GSE169695 | GEO
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:[original Title] Comparison of expression data of primary murine melanocytes from aryl hydrocarbon deficient mice and corresponding wild-type C57BL/6 mice Melanin is produced exclusively by melanocytes and melanogenesis is the vital response to protect skin cells against Ultraviolet B (UVB)-induced DNA damage. The aryl hydrocarbon receptor (AhR) is a transcription factor, which may be involved in the physiological tanning response. Normal murine melanocytes express functional AhR. We tested gene expression in WT versus AhR-deficient mice primary murine melanocytes, isolated from the skin and cultivated for several passages. Skin epidermal cells from 2 individual C57BL/6 mice and 2 individual AhR-deficient mice (deletion of exon2, AhRtm1Bra) were grown for 6-8 weeks in selection medium to propagate melanocytes.
2010-09-05 | E-GEOD-19411 | biostudies-arrayexpress