Homo sapiens
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PROVIDER: PRJNA100191 | ENA |
REPOSITORIES: ENA
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Project description:Ultraviolet B (UVB) irradiation has strong biological effects and modulates the expression of many genes. However, the major biological themes affected by UVB remain poorly understood. This work employs a loop-designed microarray approach and applies a log linear model along with multiple hypotheses testing to identify differentially regulated genes at 4, 8, 16, or 24 hours following UVB irradiation. The most prominent biological themes in lists of differentially regulated gene sets were extracted by functional enrichment analysis using DAVID bioinformatics resources 2007. By this approach, we identify that genes that participate in two prime cellular processes – the ribosome pathway and the oxidative phosphorylation pathway - are persistently activated over a period of 24 hours following UVB irradiation. Microarray results were further verified by both mitochondrial activity assay and real-time PCR analysis. These data suggest that the persistent activation of ribosome and oxidative phosphorylation pathways may have a key role in UVB-induced cellular responses. For the first time, the specific cellular pathways that respond to UVB irradiation consistently and persistently can be delineated confidently using a loop-designed microarray approach and functional bioinformatics analysis. The results of this study offer further insight into UVB-induced stress responses. Keywords: UVB, cDNA microarray, loop design, KEGG pathway
2009-04-10 | GSE7589 | GEO
Project description:The goal of this thesis is to study the response of a human keratinocyte cell line (HaCaT cells) after UVB irradiation. In order to develop a system for UV irradiation, we firtstly studied the UV illumination system to find out a stable and reliable condition for UV irradiation experiments. Further, we found out the proper dose of UVB radiation and time points after UVB irradiation by performing MTT assay and trypan blue viability test. According to the results of MTT assay and trypan blue viability test, the cellular activity as well as survival rate of UVB-irradiated cells were in proportion to the radiation doses within a lower UVB dose range. We wanted to find out the possible reasons for this phenomenon by using cDNA microarray. We hope the thesis could be a guide for the following researches, and be useful in the clinical studies about the UV damage. Keywords: dose response and time course Loop-designed microarray experiments were performed in our study. Twenty-one samples are arranges as seven small loops and one large loop, with three and seven microarray slides for each small and large loop, respectively. This set of loop-designed microarray experiment contains one control untreated (non UVB-treated) samples and two UVB-treated samples (one low dose and one high dose UVB-treated) at each time point (total seven time points).
2010-05-16 | E-GEOD-4223 | biostudies-arrayexpress
Project description:The epidermis is routinely subjected to DNA damage induced by solar (UVB) radiation. In addition to activating canonical DNA damage responses such as cycle cell checkpoints and DNA repair, UVB-induced DNA damage can also activate additional signaling pathways including inflammatory responses. The pathways activated downstream of UVB-induced DNA damage have a critical role in determining cellular survival to UVB radiation. Here we report that loss of CCAAT-enhancer/binding protein β (C/EBPβ) in mouse keratinocytes results in enhanced UVB-induced apoptosis through activation of extrinsic apoptosis genes cleaved caspase-8 and tBid. RNAseq and Ingenuity Pathway Analysis of UVB-treated C/EBPβ-/- primary keratinocytes revealed an enrichment of inflammatory signaling pathways, including the type I interferon (IFN-I) pathway as the most enriched pathway. Numerous IFN-I stimulated genes were up-regulated in UVB-treated C/EBPβ-/- keratinocytes, including genes that regulate extrinsic apoptosis. Inhibition of the interferon / receptor or the associated kinase Tyk2 greatly reduced cell death in UVB-exposed C/EBPβ deficient keratinocytes, demonstrating the dependence of IFN signaling in C/EBPβ regulated apoptosis. The apoptosis inducing cytokine, tumor necrosis factor alpha (TNF-α) was identified as one of the most significant upstream regulators activated in UVB exposed C/EBPβ-/- keratinocytes compared to UVB exposed wild type control. UVB exposed C/EBPβ-/- keratinocytes displayed increased expression of TNF-α and the enhanced apoptosis in C/EBPβ-/- keratinocytes was suppressed by a TNF-α neutralizing antibody. Our results indicate that loss of C/EBPβ enhances activation of a non-canonical UVB DNA damage response pathway involving interferon and TNF signaling to induce keratinocyte cell death.
2026-04-01 | GSE305019 | GEO
Project description:Previous studies showed that SV40 transformed cells have unique DNA damage responses; further inspecting these responses by microarray provides an opportunity to discover transciprtional insights of DNA damage responses after UVB irradiation. This study is used to comapre to GSE7589, our previous study of human normal lung fibroblast after UVB irradiation. We used a loop design in this study, cDNA microarray experiment consisted of eight RNA samples, including UVB-irradiated samples and their corresponding controls of 4 time points after UV irradiation.
2013-06-30 | E-GEOD-41319 | biostudies-arrayexpress
Project description:p53 is activated by DNA damage and oncogenic stimuli to regulate senescence, apoptosis and cell-cycle arrest, which are essential to prevent cancer. Here, we utilized UVB radiation, a potent inducer of DNA damage, p53, apoptosis and skin cancer to investigate the mechanism of CCAAT/enhancer binding protein-β (C/EBPβ) in regulating p53-mediated apoptosis in keratinocytes and to test whether the deletion of C/EBPβ in epidermis can protect mice from UVB-induced skin cancer. UVB-treatment of C/EBPβ skin conditional knockout (CKOβ) mice increased p53 protein levels in epidermis and enhanced p53-dependent apoptotic activity 3-fold compared with UVB-treated control mice. UVB increased C/EBPβ levels through a p53-dependent pathway and stimulated the formation of a C/EBPβ-p53 protein complex; knockdown of C/EBPβ increased p53 protein stability in keratinocytes. These results suggest a p53-C/EBPβ feedback loop, whereby C/EBPβ, a transcriptional target of a p53 pathway, functions as a survival factor by negatively regulating p53 apoptotic activity in response to DNA damage. RNAseq analysis of UVB-treated CKOβ epidermis unexpectedly revealed that type 1 interferon (IFN) pathway was the most highly enriched pathway. Numerous pro-apoptotic interferon stimulated genes were upregulated including some known to enhance p53 apoptosis. Our results indicate that p53 and IFN pathways function together in response to DNA damage to result in the activation of extrinsic apoptosis pathways and caspase 8 cleavage. Last, we observed CKOβ mice were resistant to UVB-induced skin cancer. Our results suggest that C/EBPβ represses apoptosis through keratinocyte autonomous suppression of the type 1 IFN response and p53 to increase cell survival and susceptibility to UVB-induced skin cancer.
2025-01-15 | GSE286963 | GEO
Project description:Sauchinone, a phenolic lignan derived from Saururus chinensis, possesses potent antioxidant and anti-inflammatory activities. Ultraviolet B (UVB) irradiation is a major environmental factor contributing to skin photoaging, primarily through the induction of oxidative stress and disruption of redox homeostasis in dermal fibroblasts. However, the transcriptional mechanisms underlying the protective effects of sauchinone against UVB-induced damage remain unclear. Human foreskin fibroblasts (HFFs) were treated with UVB irradiation in the presence or absence of sauchinone to investigate transcriptional changes, followed by RNA sequencing (RNA-seq) to analyze genome-wide gene expression profiles. We found that sauchinone treatment significantly reshaped the transcriptional landscape of UVB-exposed fibroblasts. KEGG pathway enrichment analysis revealed that differentially expressed genes were prominently enriched in signaling pathways related to inflammation, cellular stress responses, and extracellular signaling, including cytokine–cytokine receptor interaction, MAPK signaling pathway, and neuroactive ligand–receptor interaction. In addition, pathways associated with metabolic regulation and cellular communication were also affected. Notably, several genes involved in antioxidant defense and redox regulation, including downstream targets of the Nrf2 pathway, were upregulated under UVB + sauchinone conditions. These findings suggest that sauchinone exerts protective effects against UVB-induced oxidative stress at the transcriptional level and highlight its potential as a candidate antioxidant compound for mitigating photoaging-related cellular damage.
2026-05-27 | GSE326951 | GEO
Project description:Integrated multi-omics approach revealed cellular senescence landscape
| PRJNA865031 | ENA
Project description:UVB is one of the external stimuli posing a significant threat to the skin. Excessive exposure to UVB may trigger intracellular effects including inflammatory responses and oxidative stress, leading to severe skin issues. Peony seed oil is a nut oil unique to China, rich in unsaturated fatty acids, and reported to possess anti-inflammatory and antioxidant properties. Paeonia delavayi is a distinctive subspecies within the peony family, primarily distributed in southwestern China and high-altitude regions. This study aims to investigate the roles and underlying mechanisms of P. delavayi seed oil (PDSO) in protecting skin from UVB-induced damage. We found that treatment with PDSO effectively mitigated the adverse effects of UVB exposure on NHEK cells, including reduced viability and impaired migratory capacity. Additionally, PDSO significantly suppressed the upregulation of pro-inflammatory genes such as TNF, IL6, CXCL8 and PTGS2 in keratinocytes induced by UVB. Subsequent studies indicated that PDSO also alleviated UVB-induced oxidative stress and photoaging in NHEK cells, manifested by reducing ROS and MDA levels, upregulating antioxidant-related genes expression, and suppressing the expression of genes associated with cellular senescence. RNA-sequencing analysis and western blot assay revealed that PDSO exerts an inhibitory effect on the PI3K/Akt/mTOR pathway. We also found that PDSO suppressed the activation of the NF-κB pathway in UVB-irradiated NHEK cells. Thus, this study demonstrates that PDSO holds significant potential in protecting skin from UVB-induced damage and reveals that its mechanism of action involves the PI3K/Akt/mTOR and NF-κB signaling pathways.
2026-02-27 | GSE320415 | GEO
Project description:Ultraviolet (UV) radiation is a major melanoma risk factor, yet underlying mechanisms remain poorly understood. Here we introduce a mouse model permitting fluorescence-aided melanocyte imaging and isolation following in vivo UV irradiation. We use expression profiling to show that activated neonatal skin melanocytes isolated following a melanomagenic UVB dose bear a distinct, persistent interferon-response signature, including genes associated with immunoevasion. UVB-induced melanocyte activation, characterized by aberrant growth and migration, was abolished by antibody-mediated systemic blockade of interferon-gamma (IFN-gamma), but not type-I interferons. IFN-gamma was produced by macrophages recruited to neonatal skin by UVB-induced chemokine receptor Ccr2 ligands. Admixed recruited skin macrophages enhanced transplanted melanoma growth by inhibiting apoptosis; notably, IFN-gamma blockade abolished macrophage-associated melanoma growth and survival. IFN-gamma-producing macrophages were identified in 70% of human melanomas examined. Our data reveal an unanticipated role for IFN-gamma in promoting melanocytic cell survival/immunoevasion, and suggest IFN-gamma-R signaling represents a novel therapeutic melanoma target. Biologic replicates of UVA- and UVB-treated mouse melanocytes, as well as untreated mouse melanocytes and mouse keratinocytes, were used to define melanocyte expression signatures associated with UV treatment.
2011-01-01 | E-GEOD-25164 | biostudies-arrayexpress
Project description:Whole genome UV footprinting in yeast using deamination sequencing (Deam-seq), wherein photoproducts induced by high-dose UVB irradiation are revealed as mutations. In Deam-seq, cytosines within cyclobutane pyrimidine dimers (CPDs) are converted to uracil by rapid deamination at elevated temperature. Following CPD repair by photolyase, samples were sequenced at ultra-deep (>7,000×) coverage, enabling calculation of per-base damage fractions (mutant allele frequencies). By comparing cellular and naked DNA, this approach can pinpoint genomic sites bound by proteins that modulate UV damage.
2025-04-28 | E-MTAB-15116 | biostudies-arrayexpress