Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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

ORGANISM(S): Mus musculus

PROVIDER: GSE4066 | GEO | 2006/07/01

SECONDARY ACCESSION(S): PRJNA95191

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.

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

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

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

Transcriptomic analysis of grape (Vitis vinifera L.) leaves exposed to ultraviolet C radiation

2014-11-15 | GSE62315 | GEO

MiRNAs expression in supernatant after ultraviolet irradiation

Project description:To investigate the mechanism of radiation induced bystander effect, we explored miRNAs expression in supernatant of human skin fibroblasts after culturing for 24h post UV irradiation. Primary human skin fibroblasts were obtained from healthy volunteers by means of a foreskin circumcision. Human skin fibroblasts was irradiated with 20J/cm2 UVA or 60mJ/cm2 UVB. Expression of miRNAs were tested by microarray between radiation and control samples.

2018-03-07 | GSE111444 | GEO

Transcriptomic analysis of grape (Vitis vinifera L.) leaves exposed to ultraviolet C radiation

Project description:Solar ultraviolet C（UV-C）radiation reaching the Earth’s surface is little due to the filtering effects of the stratospheric ozone layer. At present, artificial UV-C irradiation is utilized for different biological processes. Grape is a major fruit crop around the world. Research has shown that UV-C irradiation induced the biosynthesis of phenols. However, changes at the molecular level in response to UV-C and leading to these effects are poorly understood. To elucidate the effect of UV-C on expression of genes in grape and the response mechanism, transcript abundance of grape (Vitis vinifera L.) leaves was quantified using the Affymetrix Grape Genome oligonucleotide microarray (15,700 transcripts) Grape leaves were exposed to UV-C irradiation at 6W/m2 for 10 min. LCK-0-1, LCK-0-2 and LCK-0-3 are 0 h after the initiation of treatment and as the controls; LTR-6-1, LTR-6-2 and LTR-6-3 are for 6 h after the initiation of treatment; LTR-12-1, LTR-12-2 and LTR-12-3 are for 12 h after the initiation of treatment. Three replicates for each time point. 9 samples in all.

2014-11-15 | E-GEOD-62315 | 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: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.

2021-08-21 | GSE182125 | GEO

Genome-wide Transcriptional Profiling of Skin and Dorsal Root Ganglia after Ultraviolet-B-Induced Inflammation

Project description:Ultraviolet-B (UVB) irradiation of the skin was performed on rat (skin and DRG) and human (skin) tissue. The resulting changes in gene expression were then profiled by using RNA-seq to compare gene expression between irradiated and non-irradiated samples

2014-03-01 | GSE54413 | GEO

Single-cell RNA-seq of UVB-radiated Skin Reveals Landscape of Photoaging-related Inflammation and Protection by Vitamin D

Project description:Due to the destruction of the ozone layer, the ultraviolet radiation received by our skin has increased significantly. Continuous exposure to sunlight can cause damage to our skin, which can lead to photoaging and even skin cancer. We performed single-cell RNA sequencing on the skin of normal and UV-irradiated mice, and found that UV-irradiation caused an inflammatory response in the skin of mice. On the contrary, the inflammation of the mice injected with vitamin D was significantly reduced. Finally, we uncovered that Hmox1 and vitamin D is related to achieve the anti-inflammatory effect of vitamin D. This provides a strategy for skin anti-UV treatment

2022-05-16 | GSE173385 | GEO

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

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