Liothyrella uva
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA314406 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR3205210_1.fastq.gz | Fastqsanger.gz | |||
| SRR3205210_2.fastq.gz | Fastqsanger.gz | |||
| SRR3205230_1.fastq.gz | Fastqsanger.gz | |||
| SRR3205230_2.fastq.gz | Fastqsanger.gz | |||
| SRR3205231_1.fastq.gz | Fastqsanger.gz |
Items per page: 5 1 - 5 of 20 |
Similar Datasets
Project description:Ultraviolet light is the dominant environmental oxidative skin stressor and a major skin aging factor. We studied which oxidized phospholipid (OxPL) mediators Ultraviolet A (UVA) would generate in primary human keratinocytes (KC). Mass spectrometric analysis of the oxidized phospholipidome of KC immediately or 24h post stress revealed dynamic changes in abundance of 174 oxidized phosphocholine species. Exposure to UVA and to in vitro UVA - oxidized phospholipids both activated, on transcriptome and proteome level, NRF2/antioxidant response signaling and lipid metabolizing enzyme expression, whereas UVA additionally initiated the unfolded protein response (UPR). We identified Nupr1 as an upstream transcriptional regulator of UVA/OxPL mediated gene expression that is itself transcriptionally regulated by reactive lipids, which also aggregate and crosslink recombinant Nupr1 protein. Nupr1 governs the basal and stress regulated expression of cell cycle, redox reactive, autophagy- and lipid metabolizing genes in epidermal keratinocytes, making it a potential key factor in skin ROS responses, -aging and -pathology.
2019-05-27 | PXD008050 | Pride
Project description:This RNA sequencing dataset analyzes circRNA expression changes in HaCaT keratinocytes after UVA irradiation. Cells were exposed to 5 J/cm2 UVA and profiled using ribosomal RNA-depleted RNA sequencing on an Illumina platform. Differentially expressed circRNAs were identified by computational pipelines. The data provide insights into circRNA regulation during photo-oxidative stress.
2024-10-02 | GSE246068 | GEO
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.
2009-06-29 | GSE15618 | GEO
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:Melanomas carry characteristic mutational signatures associated with solar UVB radiation-induced cyclobutane pyrimidine dimers (CPDs) that contain deaminated cytosines. However, there are several other mutation signatures, including those found in melanomas from non-sun-exposed body sites, that have unknown origins. To test if these signatures are linked to UVA radiation from the sun, we exposed human melanocytes to UVA and to UVB for comparison. We mapped DNA damage in the form of CPDs or 8-oxoguanine (8-oxoG) genome-wide at base resolution. We then determined mutational patterns in single melanocyte cell clones by whole genome sequencing. UVA-induced CPDs occurred overwhelmingly at TT sequences resembling melanoma signature SBS7d. We did not observe rising CPD levels after cessation of radiation (dark CPDs). However, the UVA-induced TT-CPDs did not score as mutagenic in the mutation analysis. 8-oxoG was present in melanocytes but was not substantially increased after UVA. G/C to T/A mutations were prominent in melanocyte single cell clones with no major shift after UVA radiation. These mutations matched SBS18, a signature present in melanomas. Our data suggest that melanocytes carry an endogenous but UVA-independent load of oxidative base lesions and their associated mutations that may be associated with a subset of melanoma mutations.
2025-04-16 | GSE294758 | GEO
Project description:In response to ultraviolet radiation (UVR), cells alter gene expression, switching on a variety of damage response pathways. Long non-coding RNA (lncRNA) is thought to play critical roles in regulating expression of protein-coding genes. We hypothesized that lncRNAs also regulate gene expression following UV exposure and screened for changes in lncRNA expression in human primary fibroblasts after irradiation with longwave UV (UVA) or shortwave UV (UVB).
2016-10-21 | GSE89005 | GEO
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.
2014-12-12 | E-GEOD-56754 | biostudies-arrayexpress
Project description:The effects of UV light on the skin have been extensively investigated. However, systematic information about how exposure to UVA light, the least energetic but the most abundant UV radiation reaching the Earth, shapes the subcellular organization of proteins is lacking. Using subcellular fractionation, mass-spectrometry-based proteomics, machine learning algorithms, immunofluorescence, and functional assays, we mapped the subcellular reorganization of the proteome of human keratinocytes in response to UVA light. Our workflow quantified and assigned subcellular localization and redistribution patterns for over 3000 proteins, of which about 600 were found to redistribute upon UVA exposure. Reorganization of the proteome affected modulators of signaling pathways, cellular metabolism and DNA damage response. Strikingly, mitochondria were identified as the main target of UVA-induced stress. Further investigation demonstrated that UVA induces mitochondrial fragmentation, up-regulates redox-responsive proteins and attenuates respiratory rates. These observations emphasize the role of this radiation as a potent metabolic stressor in the skin.
2022-03-06 | PXD027941 | Pride
Project description:Tissue resident macrophages play important roles in tissue homeostasis and acute response to external stimuli. Human skin equivalents (HSEs) incorporating human monocytic cell line THP-1, were fabricated to generate immunocompetent human skin models. These HSEs were used to investigate the influence of the skin microenvironment and UVA exposure on the phenotypes of macrophages. THP-1 in HSEs exhibited mixed M1 and M2 macrophage phenotypes. Transcriptomic analysis demonstrated that THP-1 in HSEs enriched extracellular matrix interaction while downregulated a DNA replication hallmark. Upon UVA exposure, immunocompetent HSEs exhibited epidermal distortion and increased DNA double-strand breaks (DSB). THP-1 isolated from UVA-exposed HSEs revealed significant upregulation of genes associated with oxidative stress, antioxidant regulation, inflammatory and UV response. A photoprotective agent, mycosporine-2-glycine (M2G), derived from cyanobacteria was applied on to immunocompetent HSEs and the responses of THP-1 cell line was investigated after UVA exposure. The result showed that UVA-induced DSB was significantly lower in M2G-treated HSEs. In addition, the inflammatory and UV response hallmarks were downregulated while the oxidative phosphorylation hallmark was upregulated in THP-1 from M2G-treated UVA exposed HSEs. Taken together, this study provides an immunocompetent 3D skin model that can be used to interrogate responses of skin resident innate immune cells to microenvironment and external stimuli such as UVA irradiation.
2024-10-01 | GSE261112 | GEO