Ontology highlight
ABSTRACT:
PROVIDER: PRJNA1048364 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR27036300_1.fastq.gz | Fastqsanger.gz | |||
| SRR27036300_2.fastq.gz | Fastqsanger.gz | |||
| SRR27036301_1.fastq.gz | Fastqsanger.gz | |||
| SRR27036301_2.fastq.gz | Fastqsanger.gz | |||
| SRR27036302_1.fastq.gz | Fastqsanger.gz |
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Project description:The UVB component of the sunlight (290-320 nm) plays an important role in carcinogenesis through generation of high levels of bipyrimidine DNA photoproducts, while UVA (320-400 nm) has been associated with photoaging and tumor progression through generation of low, but continuous levels of DNA damage and oxidative stress. However, the contribution of UVA light to epidermal cell fate in the context of photoaging remains poorly understood. Here, by using proteomic analyses and biochemical assays for validation, we show that UVA induces proteome remodeling and senescence in primary keratinocytes, eliciting potent antioxidant and pro-inflammatory responses. As a model of early skin tumorigenesis during aging, immortalized non-malignant keratinocytes, bearing potentially oncogenic mutations and dysfunctional components of the senescent machinery , are resilient to UVA-induced stress, but are sensitive to paracrine oxidative stress and immune system activation induced by senescent neighboring keratinocytes. These observations reveal a new cellular mechanism by which UVA induces photoaging in the epidermis.
2022-02-17 | PXD025191 | Pride
Project description:Considering that human skin cancer is predominantly attributed to UV radiation from sunlight, additional investigations are needed to elucidate the role of P2RY6 in UVB-induced skin carcinogenesis. Surprisingly, we find that P2ry6 deletion exhibits marked promotion to UVB-induced skin papilloma formation compared with wild-type mice, suggesting its tumor-suppressive role in UVB-induced skin cancer. Additionally, P2ry6 knockout promotes mouse skin hyperplasia induced by short-term UVB irradiation, while UDP, the ligand of P2RY6, can inhibit UVB-induced skin damage. Furthermore, UVB irradiation can significantly upregulate P2RY6 expression in mouse and human skin cells. These results indicate that P2RY6 plays a crucial protective role in resisting UVB-induced skin damage and carcinogenesis. At the molecular level, P2RY6 deletion inhibits ubiquitination and expression of XPC after UVB irradiation in keratinocytes, resulting in the accumulation of CPDs (cyclobutane pyrimidine dimers). P2RY6 deletion also activates PI3K/AKT signaling pathway in vitro and in vivo. The CPD accumulation and inflammatory responses enhanced by P2RY6 deletion are reversed by an AKT inhibitor. These findings suggest that P2RY6 acts as a tumor suppressor in UVB-induced skin cancer by regulating PI3K/AKT signaling pathway.
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Project description:Purpose: to explore the function and mechanism of skin damage induced by ultraviolet irradiation. The mouse model of UVB irradiation was established. Using miRNA Sequence analysis, the miRNA expression profile of the mouse skin model exposed to UVB radiation and the normal skin mice. GO and Pathway analysis were employed for the prediction of miRNA targets. Results:Compared with normal skin, a total of 23 miRNAs were screened for significantly different expressions. Among them, 7 miRNAs were up-regulated and 16 were down-regulated in the skin wound tissue of mice exposed to UVB irradiation. The differential expression of miRNA is related to a variety of signal transduction pathways, among which mmu-miR-195a-5p and mitogen-activated protein kinase (MAPK) signal pathway is worthy of attention. Conclusion: There was significant difference expression of miRNA in the skin tissue of normal mice and the skin injury induced by UVB irradiation. Differential expression of miRNA can be used in the diagnosis and treatment of UVB-induced acute skin injury.
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Project description:Skin aging caused by UV is called photoaging, which is characterized by deeper wrinkles accompanied by senescence of dermal fibroblasts and reduction of collagens. Rice fermentation, widely used in the cosmetics, has been reported to possess anti-aging benefits on skincare, however, its roles in the skin photoaging remains unclear. In this study, the effects of Maifuyin (a rice fermentation), and its ingredients succinic acid (SA) and choline on UVA-induced senescence in fibroblasts were evaluated. A mRNA sequencing technology (RNA-seq) was applied to study the effects of these ingredients on UVA-induced photoaging. In conclusion, these results highlight the potential use of Maifuyin and SA as promising agents for anti-photoaging applications.
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Project description:Occurrence and mechanism of photoaging in mouse back skin
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Project description:UV-induced CPDs were mapped in primary skin melanocytes or normal human skin fibroblasts following either UVC or UVB irradiation and in isolated human genomic DNA (naked DNA control) that was UVB or UVC irradiated. CPDs were mapped across the human genome using the CPD-capture-seq method and the resulting libraries were captured for ~4000 genomic regions of interest (~3 Mbp) of the human genome by the company Rapid Genomics prior to Illumina sequencing
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Project description:Background: Atopic dermatitis (AD) is a common inflammatory skin disease with broad impact on quality of life and on the health care system. The pathophysiology is not fully understood, but it is likely multifactorial involving immune dysfunction, altered skin barrier and environmental factors. Narrow band ultraviolet B (nb-UVB) treatment leads to normalization of the tissue and clinical improvement. However, knowledge of early changes in AD skin in response to nb-UVB is lacking and could provide important clues to decipher the disease mechanisms and potential new treatment targets. Objective: To map the early transcriptional changes in the skin in response to nb-UVB treatment. Results: When examining the early response after only three local UVB-treatments, gene expression analysis revealed 30 down- and 47 up-regulated transcripts. Among these only a small proportion were related to the inflammatory response. Interestingly, two cytokines of the interleukin (IL)-1 family were differentially expressed: the proinflammatory cytokine IL-36γ was reduced after treatment, while the anti-inflammatory cytokine IL-37 increased in skin after treatment with nb-UVB. Conclusion: Local nb-UVB induced an early decrease of the pro-inflammatory cytokine IL-36γ and an increase of the anti-inflammatory IL-37. This likely represents one of the first changes in inflammatory signaling induced by nb-UVB in atopic eczema.
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