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PROVIDER: PRJNA977685 | ENA |
REPOSITORIES: ENA
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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
Project description:Long wavelength Ultraviolet (UVA-1) radiation causes oxidative stress that leads to the formation of noxious substances within the skin. As a defensive mechanism skin cells produce detoxifying enzymes and antioxidants when they detect modified molecules. We have recently shown that UVA-1 irradiation oxidizes the abundant membrane phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC), which then induced the synthesis of the stress response protein heme oxygenase 1 (HO-1) in dermal fibroblasts. Here we examined the effects of UVA-1 and (UV-) oxidized phospholipids on the global gene expression in human dermal fibroblasts. We identified a cluster of genes that were co-induced by UVA-1-oxidized PAPC and UVA-1 radiation. The cluster included HO-1, glutamate-cysteine ligase modifier subunit (GCLM), aldo-keto reductases-1-C1 and -C2 (AKR1C1, AKR1C2), and interleukin 8 (IL8). These genes are members of the cellular stress response system termed âantioxidant responseâ or âPhase II detoxificationâ. Accordingly, the regulatory regions of all these genes contain binding sites for NF-E2-related factor 2 (Nrf2), a major regulator of the antioxidant response. Both UVA-1 irradiation and treatment with oxidized lipids led to increased nuclear accumulation of Nrf2. Silencing expression of Nrf2 using siRNA or using cells and tissue from Nrf2-deficient mice, we show that the induction of the co-regulated genes was suppressed. Expression of other canonical UVA-1-induced genes, including cyclooxygenase 2 (Cox2) and interleukin 6 (IL6) was unaltered in the absence of Nrf2. Together, our data show that UVA-1-mediated lipid oxidation induces induction of antioxidant response genes, which is dependent on the redox-regulated transcription factor Nrf2. To activate Nrf2 is a major strategy for novel antioxidant drugs, the skin photo-adaptation (SPA) inducers. Our finding that specific uv-oxidized lipids act similar sheds a new (ultraviolet) light on the usually detrimental âimageâ of UV generated lipid mediators. Experiment Overall Design: we profiled global mRNA expression levels in human dermal fibroblasts that had been treated with either UVA-1 or oxidized lipids. To investigate the effect of oxidized phospholipids on gene regulation, we used two preparations, which differed in their degree of oxidation; the minimally oxidized UV-PAPC resulting from UVA-1 irradiation of PAPC, and air-oxidized PAPC (OxPAPC), which represents the full spectrum of oxidation products (Gruber 07) (Reis et al., 2005). We irradiated dermal fibroblasts with UVA-1 (40J/cm²) or treated them with UV-PAPC, OxPAPC or native PAPC (100µg/ml each). We analyzed global gene expression four hours after stimulation with gene arrays (Affymetrix U133A Plus 2.0 Gene Chips).
2009-11-10 | E-GEOD-13606 | biostudies-arrayexpress
Project description:Ultraviolet (UV) radiation from the sun causes adverse skin changes such as premature aging. UV-induced mitochondrial DNA (mtDNA) alterations, including deletions, contribute to photoaging and cellular dysfunction. The most frequent mtDNA rearrangement is the common deletion (CD), characterized by the loss of nearly one-third of the genome (4,977 bp). Although UV radiation exposure leads to CD formation, the molecular mechanisms initiating UV-induced CD remain poorly defined. In this study, we show that increasing UV doses increase CD levels in human skin fibroblasts. UVA exposure increased cellular reactive oxygen species (ROS) and mtDNA oxidation. Antioxidant preconditioning prevented UVA-induced CD accumulation, indicating a ROS-dependent mechanism. Conversely, UVB exposure induced cyclobutane pyrimidine dimers (CPDs) without affecting ROS, suggesting a ROS-independent pathway. Using a 3D full-thickness human skin model, we confirmed UVA-dependent CD formation in both epidermis and dermis. RNA-Seq analysis of UVA-exposed fibroblasts revealed upregulation of mitochondrial DNA replication genes and downregulation of mtDNA repair genes. Taken together, our findings provide insight into how UVA and UVB differ in their detrimental effects on mtDNA, with UVA impacting mtDNA maintenance and transcription via a ROS-dependent mechanism.
2025-11-30 | GSE302943 | GEO
Project description:UVA radiation is one of the main harmful factor that penetrates all human skin layers and influencing communication between the cells that build them. To prevent UVA-induced damage, there is a constant search for compounds that could protect all skin cells, as well as restoring homeostasis in their communication. Therefore, the aim of this study was to evaluate the effect of 3-O-ethyl ascorbic acid (EAA) on the intracellular proteome of co-cultured keratinocytes and fibroblasts after UVA irradiation and on the profile of proteins released into the medium by both cell types. Proteomic approach allowed to identify significantly modified by UVA as well as EAA proteins. In keratinocytes UVA radiation enhanced expression of pro-inflammatory and pro-proliferative/keratinizing proteins and decreased anti-apoptotic and antioxidant proteins, while in fibroblasts UVA radiation induced expression mainly of proinflammatory proteins, simultaneously decreasing the level of proteins involved in antioxidant response, as well as growing factors. Similar effect was observed in the medium of co-cultured cells, where increase in pro-inflammatory protein and decrease in growing factors were observed. Medium supplementation with EAA restored the levels of these proteins compared to control cultures. The results of this study show that EAA may act as a protector of epidermal and dermal cells, because it reduces the levels of pro-inflammatory proteins and increases the activity of the antioxidant system of skin cells (keratinocytes and fibroblasts), as well as normalizes intercellular signaling.
2026-08-24 | PXD071840 | Pride
Project description:Long wavelength Ultraviolet (UVA-1) radiation causes oxidative stress that leads to the formation of noxious substances within the skin. As a defensive mechanism skin cells produce detoxifying enzymes and antioxidants when they detect modified molecules. We have recently shown that UVA-1 irradiation oxidizes the abundant membrane phospholipid 1-palmitoyl-2-arachidonoyl-sn-glycero-3-phosphorylcholine (PAPC), which then induced the synthesis of the stress response protein heme oxygenase 1 (HO-1) in dermal fibroblasts. Here we examined the effects of UVA-1 and (UV-) oxidized phospholipids on the global gene expression in human dermal fibroblasts. We identified a cluster of genes that were co-induced by UVA-1-oxidized PAPC and UVA-1 radiation. The cluster included HO-1, glutamate-cysteine ligase modifier subunit (GCLM), aldo-keto reductases-1-C1 and -C2 (AKR1C1, AKR1C2), and interleukin 8 (IL8). These genes are members of the cellular stress response system termed “antioxidant response” or “Phase II detoxification”. Accordingly, the regulatory regions of all these genes contain binding sites for NF-E2-related factor 2 (Nrf2), a major regulator of the antioxidant response. Both UVA-1 irradiation and treatment with oxidized lipids led to increased nuclear accumulation of Nrf2. Silencing expression of Nrf2 using siRNA or using cells and tissue from Nrf2-deficient mice, we show that the induction of the co-regulated genes was suppressed. Expression of other canonical UVA-1-induced genes, including cyclooxygenase 2 (Cox2) and interleukin 6 (IL6) was unaltered in the absence of Nrf2. Together, our data show that UVA-1-mediated lipid oxidation induces induction of antioxidant response genes, which is dependent on the redox-regulated transcription factor Nrf2. To activate Nrf2 is a major strategy for novel antioxidant drugs, the skin photo-adaptation (SPA) inducers. Our finding that specific uv-oxidized lipids act similar sheds a new (ultraviolet) light on the usually detrimental “image” of UV generated lipid mediators.
2009-10-22 | GSE13606 | GEO
Project description:Melanomas carry characteristic mutational signatures associated with solar UVB radiation-induced cyclobutane pyrimidine dimers (CPDs) that contain deaminated cytosines. However, there are several other mutation signatures, including those found in melanomas from non-sun-exposed body sites, that have unknown origins. To test if these signatures are linked to UVA radiation from the sun, we exposed human melanocytes to UVA and to UVB for comparison. We mapped DNA damage in the form of CPDs or 8-oxoguanine (8-oxoG) genome-wide at base resolution. We then determined mutational patterns in single melanocyte cell clones by whole genome sequencing. UVA-induced CPDs occurred overwhelmingly at TT sequences resembling melanoma signature SBS7d. We did not observe rising CPD levels after cessation of radiation (dark CPDs). However, the UVA-induced TT-CPDs did not score as mutagenic in the mutation analysis. 8-oxoG was present in melanocytes but was not substantially increased after UVA. G/C to T/A mutations were prominent in melanocyte single cell clones with no major shift after UVA radiation. These mutations matched SBS18, a signature present in melanomas. Our data suggest that melanocytes carry an endogenous but UVA-independent load of oxidative base lesions and their associated mutations that may be associated with a subset of melanoma mutations.
2025-04-16 | GSE294758 | GEO
Project description:Ultraviolet A (UVA) radiation is the major fraction of UV radiation reaching the Earth’s surface; its harmful effects on microorganisms obey mainly to oxidative damage, with the consequent loss of bacterial viability. In this work, the global transcriptional response of Pseudomonas aeruginosa exposed to UVA was analyzed. P. aeruginosa is an opportunistic human pathogen, also present in terrestrial and aquatic environments; its high ubiquity and versatily obeys to a complex regulatory network wich allows it to adapt to stressful conditions. To conduct this study, the PAO1 strain was grown in under sublethal doses of UVA or in the dark up to early logarithmic phase, and total RNA was obtained and sequenced by the RNA-seq technique. The analysis of the results, taking as significant a factor change ≥ 2 between irradiated and control samples, indicated that a total of 298 genes were regulated by UVA, representing 5.36 % of the total P. aeruginosa genome; half of these were induced and the other half were repressed. Data obtained by the transcriptomic study were validated by using RT qPCR of selected genes. The results presented in this study suggest that one of the main UVA targets are proteins carrying [Fe-S] clusters since several genes involved in the processes of synthesis, trafficking and assembly of these structures were upregulated. The management of intracellular iron levels also seems to be a robust response to this stress factor. The strong induction of genes involved in denitrification led us to suggest that this pathway and/or reactive nitrogen species such as nitric oxide could have a role in the response to this radiation. DNA also demonstrated to be an important UVA target as observed by the induction of SOS, prohage and pyocins genes. On the other hand, the down-regulation of genes involved in the biosynthesis of PQS, a quorum sensing signal of P. aeruginosa with several functions, could be beneficial given its role as endogenous photosensitizer. The study of the effects of UVA radiation is interesting due to its ecological consequences in natural environments. In addition, taking into account the high sensitivity of P.aeruginosa to UVA radiation and the issues with using traditional antibacterial products by the intrinsec or acquired resistance of P. aeruginosa to these agents, specially in the case of biofilms, UVA studies could have important implications for human health, industrial facilities and environmental management.
2024-10-22 | E-MTAB-13681 | biostudies-arrayexpress