Ontology highlight
ABSTRACT:
PROVIDER: PRJNA917200 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR22956007_1.fastq.gz | Fastqsanger.gz | |||
| SRR22956007_2.fastq.gz | Fastqsanger.gz |
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Project description:Primary human epidermal keratinocytes were exposed to in-vitro UVA-oxidized 1-palmitoyl-2-arachidonoyl-phosphatidylcholine or to UVA in presence and absence of a commercial UVA filter.
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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.
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.
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Project description:Transcriptional analysis of staged leaf bud tissue during dormancy and bud-break in blackcurrant using SCRI custom Ribes 4k arrays
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Project description:E. coli growing in continuous culture under continuous UVA irradiation exhibits growth inhibition with a subsequent adaptation to the stress. Transcriptome analysis was performed during transient growth inhibition and in the UVA light-adapted growth state. The results indicate that UVA light induces stringent response and an additional response that includes the upregulation of the synthesis of valine, isoleucine, leucine, phenylalanine, histidine and glutamate. The induction of several SOS response-genes strongly points to DNA damage as a result of UVA exposure. The involvement of oxidative stress was observed with the induction of ahpCF. Taken together it supports the hypothesis of the production of reactive oxygen species by UVA light. In the UVA-adapted cell population strong repression of the acid tolerance response was found. We identified the enzyme chorismate mutase as a possible chromophore for UVA light-inactivation and found strong repression of the pyrBI operon and the gene mgtA encoding for an ATP dependent Mg2+ transporter. Furthermore, our results indicate that the role of RpoS may not be as important in the adaptation of E. coli to UVA light as it was implicated by previous results with starved cells, but that RpoS might be of crucial importance for the resistance under transient light exposure. Keywords: stress response
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Project description:The aim of the measurements was to investigate RNA damage and RNA-protein crosslinks (RPC) formation in the context of aldehyde-induced toxicity. For this, a photoactivatable-ribonucleoside-enhanced crosslinking (PAR-CL) strategy using 4-thiouridine (4-SU) and UVA-radiation was used. The submitted dataset contains data from LC-MS/MS measurements of crosslinks between proteins and poly-adenylated mRNAs (mRPCs). The measurements included the following six samples sets: Sample set 1 (9 runs = 3 conditions in 3 replicates): RPCs after formaldehyde (FA) and 4-SU + UVA treatment isolated using the protein-x-linked RNA extraction (XRNAX) protocol (doi:10.1016/j.cell.2018.11.004) Conditions: RPCs from untreated HAP1 =Ctrl RPCs from HAP1 treated with FA RPCs from HAP1 treated with 4-SU + UVA Sample set 2 (12 runs = 4 conditions in 3 replicates): mRPCs after 4-SU + UVA treatment using poly-A pulldown Conditions: mRPCs from untreated HAP1=Ctrl mRPCs from HAP1 treated with UVA but without 4-SU (0h after irradiation) mRPCs from HAP1 treated with 4-SU but without UVA mRPCs from HAP1 treated with 4-SU + UVA (0h after irradiation) Sample set 3 (24 runs = 6 conditions in 4 replicates): mRPCs after 4-SU + UVA and Ub-E1i treatment using poly-A pulldown Conditions: mRPCs from HAP1 treated with 4-SU + UVA (0h, 0.5h and 1h after irradiation) mRPCs from HAP1 treated with 4-SU + UVA and Ub-E1i (0h, 0.5h and 1h after irradiation) Sample set 4 (24 runs = 6 conditions in 4 replicates): mRPCs after 4-SU + UVA and MG132 treatment isolated using poly-A pulldown Conditions: mRPCs from HAP1 treated with 4-SU + UVA (0h, 0.5h and 1h after irradiation) mRPCs from HAP1 treated with 4-SU + UVA and MG132 (0h, 0.5h and 1h after irradiation) Sample set 5 (24 runs = 6 conditions in 4 replicates): mRPCs after 4-SU + UVA and ANS treatment using isolated poly-A pulldown Conditions: mRPCs from HAP1 treated with 4-SU + UVA (0h, 0.5h and 1h after irradiation) mRPCs from HAP1 treated with 4-SU + UVA and ANS (0h, 0.5h and 1h after irradiation) Sample set 6 (24 runs = 6 conditions in 4 replicates ): mRPCs after 4-SU+UVA in AAVS1 control and RNF14 KO cells using poly-A pulldown mRPCs from HAP1 AAVS1 control cells (clone #6) treated with 4-SU+UVA (0h, 0.5h and 1h after irradiation) mRPCs from HAP1 RNF15 KO cells (clone #15) treated with 4-SU+UVA (0h, 0.5h and 1h after irradiation) Abbreviations: 4-SU: 4-thiouridine ANS: Anisomycine, a translation elongation inhibitor FA: Formaldehyde MG132: proteasome-inhibitor mRPCs: crosslinks between proteins and poly-adenylated mRNAs isolated by Poly-A pulldown RPCs: crosslinks between proteins and RNA isolated by XRNAX Ub-E1i: ubiquitin E1 inhibitor (E1i, TAK-243) UVA: Ultraviolet A
2023-11-03 | PXD038332 | 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.
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