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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

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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

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

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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.

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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]

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

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