Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

How does the skin respond to genotoxic stress: The programmed gene expression change in C57BL/6 mice after ultraviolet radiation damage

ABSTRACT: Ultraviolet (UV) radiation is a major source of skin damage. It is important to define the programmed gene expression change after UV exposure, particularly in the C57BL/6 lab mice model. Here we systematically analyze the acute gene expression change in mouse skin after UV exposure.

ORGANISM(S): Mus musculus

PROVIDER: GSE182125 | GEO | 2021/08/21

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.

2006-07-01 | GSE4066 | GEO

Erbb2 regulates inflammation and proliferation in the skin after ultraviolet irradiation.

Project description:Exposure to ultraviolet (UV) irradiation is the major cause of nonmelanoma skin cancer, the most common form of cancer in the United States. UV irradiation has a variety of effects on the skin associated with carcinogenesis, including DNA damage and effects on signal transduction. The alterations in signaling caused by UV regulate inflammation, cell proliferation, and apoptosis. UV also activates the orphan receptor tyrosine kinase and proto-oncogene Erbb2 (HER2/neu). In this study, we demonstrate that the UV-induced activation of Erbb2 regulates the response of the skin to UV. Inhibition or knockdown of Erbb2 before UV irradiation suppressed cell proliferation, cell survival, and inflammation after UV. In addition, Erbb2 was necessary for the UV-induced expression of numerous proinflammatory genes that are regulated by the transcription factors nuclear factor-kappaB and Comp1, including interleukin-1beta, prostaglandin-endoperoxidase synthase 2 (Cyclooxygenase-2), and multiple chemokines. These results reveal the influence of Erbb2 on the UV response and suggest a role for Erbb2 in UV-induced pathologies such as skin cancer. Keywords: time course, ultraviolet irradiation, UV, erbB2, mouse skin The dorsal skin of adult female CD-1 mice was clipped one day before treatment and shaved on the day of treatment. DMSO or 4 mg AG825 dissolved in DMSO was applied topically to the shaved back of the mice 2 h prior to exposure to 10 kJ/m^2 UV or sham irradiation. The UV dose was approximately 30% UVA, 70% UVB and <1% UVC, with a total output of 470 uW/cm^2. Flash frozen skin was removed and total RNA expracted with TRIzol reagent (Invitrogen) and further purified with an RNeasy kit (Qiagen). Amplification, reverse-transcription, biotinylation, and hybridization were all carried out under standard conditions and procedures recommended by the manufacturer.

2006-07-01 | E-GEOD-4066 | biostudies-arrayexpress

How does the skin respond to genotoxic stress: The programmed gene expression change in C57BL/6 mice after ultraviolet radiation damage

Project description:How does the skin respond to genotoxic stress: The programmed gene expression change in C57BL/6 mice after ultraviolet radiation damage

| PRJNA754658 | ENA

Transcriptome Analysis in Mouse Skin After Exposure to Ultraviolet Radiation from a Canopy Sunbed

Project description:Exposure of skin to ultraviolet radiation (UV-R), in the form of both natural and artificial tanning, strongly increases the risk for developing skin cancer. On a molecular level, exposing cells and tissues to UV-R results in well-documented transcriptional changes. However, many of the previous investigations into these transcriptional responses did not adequately characterize the UV emissions or only assessed a limited number of doses or post-exposure times. As a result, our objectives were to provide a mechanistic study that describes the dose- and time-dependent changes in gene expression that drive adverse short-term (e.g. sunburn) and long-term actinic (e.g. skin cancer) possibly delineating response thresholds. In the current study, we examined transcriptomic expression data from mouse skin following exposure to five erythemally-weighted doses (0, 5, 10, 20, 40 mJ/cm2) of UV-R emitted from a UV-emitting tanning device, with six post-exposure durations of 0, 6, 24, 48, 72 and 96 hours (h). Surprisingly, the lowest sub-erythemal dose of 5 mJ/cm2, produced 116 significant DEGs at 96 h post-exposure related to genes associated with structural changes associated with UV-R damage. The largest number of significant changes in gene expression were found at the 6 and 48 h post-exposure time points at the doses of 20 and 40 mJ/cm2. At the highest dose of 40 mJ/cm2, 13 differentially expressed genes of interest were commonly perturbed across all post-exposure time points relative to the time-matched control groups. UV-R exposure induced pathways related to oxidative stress, P53 signaling, inflammation, biotransformation, skin barrier maintenance and innate immunity. The transcriptional data generated in this in vivo study provides mechanistic insight into the short-term and potential long-term health effects of exposure to UV-R tanning that may not be threshold dependent.

2024-10-01 | GSE245747 | GEO

Ultraviolet light induces HERV expression to activate RIG-I signaling pathway in keratinocytes

Project description:Skin inflammation and photosensitivity are common in lupus erythematosus (LE) patients, and Ultraviolet (UV) light is a known trigger of skin and possibly systemic inflammation in systemic lupus erythematosus (SLE) and discoid lupus erythematosus (DLE) patients. Type I interferons (IFN) are upregulated in LE skin after UV exposure, however, the mechanisms to explain UVB-induced inflammation remain unclear. Here we performed RNA-seq to HaCat cells with UVB irradiation to characterize gene expression and resolve differential responses of keratinocytes, in order to understand how the keratinocyte response contributes to the disease. Our data showed that HERVs and RIG-I pathway were activated in keratinocytes after UVB exposure and indicate that RIG-I pathway and HERVs are involved in proinflammatory by activating the I-IFN pathway, which provide a novel insight into how UVB promotes and aggravate skin lesion of LE patients.

2022-05-01 | GSE198792 | GEO

Differential Expression Profiles and Function Predictions for tRFs & tiRNAs in Skin Injury Induced by Ultraviolet Irradiation

Project description:Purpose: to explore the function and mechanism of skin damage induced by ultraviolet irradiation. Method: Skin tRF & tiRNA profiles of mice normal skin and damage skin induced by Ultraviolet Irradiation (UV) were generated by deep sequencing, using Illumina NextSeq 500. qRT–PCR validation was performed using SYBR Green assays. Results:Sequencing was used to screen expression profiles and predict target genes. Compared with normal skin, a total of 31 differentially expressed tRFs and tiRNAs were screened. Among these, 10 tRFs and tiRNAs were shown to be significantly different in expression levels, where there were 4 up-regulated and 6 down-regulated target genes.Altered expression of 4 genes was confirmed with qRT–PCR, demonstrating the high degree of sensitivity of the RNA-seq method. Hierarchical clustering of differentially expressed genes uncovered several as yet uncharacterized genes that may contribute to skin repair after damage induced by ultraviolet irradiation. Conclusion: tRF-Trp-TCA-001 and tRF-Gly-CCC-019 plays an important role in acute skin injury induced by UVB radiation by regulating the ras-related C3 botulinum toxin substrate 1 (Rac1) gene in the WNT signaling pathway. This study provides new insights into the mechanisms and therapeutic targets of UV-induced skin injury.

2021-08-06 | GSE162641 | GEO

The early local and systemic Type I interferon responses to ultraviolet B light exposure are cGAS dependent.

Project description:Most systemic lupus erythematosus (SLE) patients are photosensitive and ultraviolet B light (UVB) exposure worsens cutaneous disease and precipitates systemic flares of disease. The pathogenic link between skin disease and systemic exacerbations in SLE remains elusive. In an acute model of UVB-triggered inflammation, we observed that a single UV exposure triggered a striking IFN-I signature not only in the skin, but also in the blood and kidneys. The early IFN-I signature was significantly higher in female compared to male mice. The early IFN-I response in the skin was almost entirely, and in the blood partly, dependent on the presence of cGAS, as was skin inflammatory cell infiltration. Inhibition of cGAMP hydrolysis augmented the UVB-triggered IFN-I response. UVB skin exposure leads to cGAS-activation and both local and systemic IFN-I signature and could contribute to acute flares of disease in susceptible subjects such as patients with SLE.

2020-04-13 | GSE148535 | GEO

Solar simulated ultraviolet radiation induces histone 3 methylation changes in the gene promoters of matrix metalloproteinases 1 and 3 in primary human dermal fibroblasts [II]

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

Solar simulated ultraviolet radiation induces histone 3 methylation changes in the gene promoters of matrix metalloproteinases 1 and 3 in primary human dermal fibroblasts [I]

2014-08-27 | GSE60794 | GEO

UVB drives transcriptomic and epigenetic reprogramming which can be protected by antioxidant sulforaphane in human skin keratinocytes [RNA-seq]

Project description:Continuous exposure to ultraviolet (UV) is one of the main factors contributing to skin carcinogenesis. Sulforaphane (SFN) is a potent antioxidative agent which has potential to prevent the UV-induced skin cell transformation. We characterized the transcriptome and CpG methylation profile of human keratinocytes (HaCaT cells) treated with UVB and/or SFN using RNA sequencing.

2021-10-07 | GSE185320 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data