Ontology highlight
ABSTRACT:
PROVIDER: PRJNA888347 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR21844700_1.fastq.gz | Fastqsanger.gz | |||
| SRR21844700_2.fastq.gz | Fastqsanger.gz | |||
| SRR21844701_1.fastq.gz | Fastqsanger.gz | |||
| SRR21844701_2.fastq.gz | Fastqsanger.gz | |||
| SRR21844702_1.fastq.gz | Fastqsanger.gz |
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Project description:Ultraviolet (UV) wavebands in sunlight are immunomodulatory. About half the amount of UVA within a minimum erythemal dose of sunlight is systemically immunosuppressive, while higher doses protect from UVB immunosuppression in mice. We have previously shown that these responses to UVA are genetically restricted as they occur in C57BL/6 but not Balb/c mice. We used gene set enrichment analysis of microarray data and real-time RT-PCR confirmation to determine the molecular mechanisms associated with UVA immunomodulation. We found up-regulation of mRNA for the alternative complement pathway. The core-enriched genes complement component 3, properdin and complement factor B were all activated by the immunosuppressive dose of UVA only in UVA-responsive C57BL/6 but not unresponsive BALB/c mice. This therefore matched the genetic restriction and dose responsiveness of UVA immunosuppression. The immune-protective higher UVA dose prevented UVB from down regulating chemokine receptor 7 and IL-12B, and decreased IL-10, supporting previous identification of IL-12 and IL-10 in high dose UVA protection from UVB immunosuppression. Our study has identified activation of the alternative complement pathway as a trigger of UVA-induced systemic immunosuppression and suggests that this pathway is likely to be an important sensor of UVA-induced damage to the skin. 24 hours after UVA, UVB and ssUV irradiation, a 1 cm2 uniform section of skin was excised from the dorsal surface of irradiated and control mice. Total RNA was then extracted from the whole skin using TRIzol reagent (Gibco Invitrogen Life Technologies, Carlsbad, CA, USA) according to the manufacturerâ??s instructions, purified, DNase treated and reverse transcribed into cDNA. For the microarray study a direct incorporation of Cyanine 3-dCTP and Cyanine 5-dCTP fluorescent dyes (Perkin Elmer Life Sciences, Inc. Boston, MA, USA) was used for cDNA synthesis. For each UV dose, a reference design was used to compare an unirradiated control against an irradiated sample. Microarray experiments used compugen 22k mouse oligonucleotide microarray slides (The Clive and Vera Ramaciotti Centre for Gene Function Analysis, Sydney Australia (http://www.ramaciotti.unsw.edu.au). Lower and higher UVA doses were used. C57BL/6 mice were irradiated with lower UVA, higher UVA, UVB, or ssUV; Balb/C mice were irradiated with lower or higher UVA. Experiments were replicated 6 times for each UV dose. A fluorescent dye swap was done for each alternate hybridisation to reduce systematic dye bias of incorporated fluorescent dyes.
2010-05-16 | E-GEOD-15618 | biostudies-arrayexpress
Project description:To test whether there is a photoprotective benefit after different types of suberythemal repetitive UV, a 1.5 MED challenge dose was applied 1 week after the initial 2 weeks of repetitive irradiation. To determine what different mechanisms and/or factors might be involved in physiological pigmentary responses of the skin to different types of UV, we used whole human genome microarrays and immunohistochemical analyses to characterize human skin in situ to examine how melanocyte-specific proteins and paracrine melanogenic factors are regulated by repetitive exposure to suberythemal doses of different types of UV (UVA and/or UVB). Seven volunteers with skin type II-III were irradiated with UVA, UVB or UVA+UVB radiation for 2 weeks (5 times per week, 10 times total) after preliminary determination of their MEDs. A UVA+UVB challenge dose of 1.5X the MED was applied 1 week later. Biopsies were taken before the challenge dose, immediately after the challenge dose, 4 days after the challenge, and 15 weeks after the challenge.
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Project description:Ultraviolet (UV) wavebands in sunlight are immunomodulatory. About half the amount of UVA within a minimum erythemal dose of sunlight is systemically immunosuppressive, while higher doses protect from UVB immunosuppression in mice. We have previously shown that these responses to UVA are genetically restricted as they occur in C57BL/6 but not Balb/c mice. We used gene set enrichment analysis of microarray data and real-time RT-PCR confirmation to determine the molecular mechanisms associated with UVA immunomodulation. We found up-regulation of mRNA for the alternative complement pathway. The core-enriched genes complement component 3, properdin and complement factor B were all activated by the immunosuppressive dose of UVA only in UVA-responsive C57BL/6 but not unresponsive BALB/c mice. This therefore matched the genetic restriction and dose responsiveness of UVA immunosuppression. The immune-protective higher UVA dose prevented UVB from down regulating chemokine receptor 7 and IL-12B, and decreased IL-10, supporting previous identification of IL-12 and IL-10 in high dose UVA protection from UVB immunosuppression. Our study has identified activation of the alternative complement pathway as a trigger of UVA-induced systemic immunosuppression and suggests that this pathway is likely to be an important sensor of UVA-induced damage to the skin.
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Project description:Skin cancer is the most prevalent cancer in humans, especially in the United States, Australia, and New Zealand. Australia and New Zealand are the two countries with the highest rates of skin cancer in the world, about four times higher than the United States, the United Kingdom and Canada. According to statistics, one American dies of skin cancer every hour. Studies have shown that ultraviolet radiation is the main cause of skin cancer, and ultraviolet rays are mainly divided into UVA, UVB and UVC according to wavelength, UVA and UVB can cause DNA damage, and UVB is the main factor that induces skin cancer. UVB is primarily a direct damage to cellular DNA and generally includes the formation of pyrimidine dimers (CPDs) and 6-4 photoproducts (6-4PPs). UVB can also cause mutations in tumor suppressor genes such as p53, ptch, and ras. These bases the mutation will promote the activation of related signaling pathways, thereby inducing the production of tumors.In this study, we will use gene chip technology to screen out UVB-sensitive genes, and then select the genes of the UVB-sensitive GPCR family from these genes, and further use PCR for verification, so as to identify UVB-sensitive GPCRs, which will provide a basis for further experimental research.
2024-01-16 | GSE251673 | GEO
Project description:The selection of specific miRNAs by exosomes and their release from cultured melanocytes after exposure to solar UVR (UVA+UVB) have activities in inducing these cells into a premature senescence.
2020-06-01 | GSE141618 | 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:To test the hypothesis that different mechanisms and/or factors might be involved in physiological pigmentary responses of the skin to different types of UV, we used whole human genome microarrays and immunohistochemical analyses to characterize human skin in situ to examine how melanocyte-specific proteins and paracrine melanogenic factors are regulated by repetitive exposure to suberythemal doses of different types of UV (UVA, UVB or SSR). Six volunteers with skin type II-III were irradiated with SSR, UVA or UVB radiation for 2 weeks (5 times per week, 10 times total) after preliminary determination of their MEDs. Biopsies were taken 3 days after the last irradiation.
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Project description:The aim of this study was to analyze the changes in the proteomic profile of plasma from chronically UVA or UVB irradiated rats and define the effect on these changes of skin topically applied CBD.
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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.
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