RNA-Seq analysis to assess gene expression levels in MDA-MB-231 cells on treatment with (5-oxo-2-dibenzothienylmethyl)triphenylphosphonium (1-SO) and (2-dibenylthienylmethyl)triphenylphosphonium (1-S) under different UV-A irradiation conditions
Ontology highlight
ABSTRACT:
ORGANISM(S): Homo sapiens
PROVIDER: GSE154809 | GEO | 2020/11/17
REPOSITORIES: GEO
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Project description:comparison of gene expression between UV-B irradiated Physcomitrella patens gametophores with their non-irradiated controls in two different UV irradiation fields.
2010-04-28 | E-MEXP-2508 | biostudies-arrayexpress
Project description:Dr. Liu's research group is interested in studying the expression and functions of galectin-3, -7 and -12, in particular the roles of these proteins in inflammation and neoplasm. Members of the galectin family are known to participate in cellular homeostasis by modulating cell growth, controlling cell cycle progression, and inducing or inhibiting apoptosis. It is known that some galectins have similar functions. However, it is not fully understood whether they work cooperatively or not. As the outermost barrier of the body, skin is directly and frequently exposed to a prooxidative environment, including solar ultraviolet A (UVA), ultraviolet B (UVB) radiation, and air pollution. Several reports have shown that exposure of cells to UV increase or decrease the levels of galectins. For example, the amounts of galectin-7 mRNA and protein are increased rapidly after UVB irradiation of keratinocytes (Proc. Natl. Acad. Sci. USA 1999; 96:11329-34). Heat shock and subculturing decrease, while alkylating agents and UV-light increase galectin-3 (Cell Physiol Biochem 2000; 10:149-58). To analyze the change of all galectin gene expression profiles after UVB irradiation and to determine the presence or absence of coordinate regulation, we analyzed the gene expression profiles of keratinocytes exposed to UVB. Normal human epidermal keratinocytes (NHEK) were irradiated with 200 J/m2 of UVB. Total RNA will be extracted at 0, 6, 12 and 24 h after irradiation (duplicate) for analysis on the Glyco gene chip. Several reports have shown that exposure to UV light can regulate levels of galectin in skin. This study seeks to analyze the changes in all galectin gene expression profiles post-UVB irradiation to determine the presence or absence of coordinate regulation. In this study, normal human keratinocytes were irradiated with 200J/m2 of UVB. Total RNA was extracted at 0, 6, 12, and 24-hour post irradiation time points, in duplicate. Samples were hybridized and analyzed using the GLYCOv2 array.
2011-02-17 | E-GEOD-27360 | biostudies-arrayexpress
Project description:Titanium dioxide (TiO2) based nanomaterials (NMs) are among the most produced NMs worldwide. When irradiated with light, particularly UV, TiO2 is photoactive, a property that is explored for several purposes. There is an increasingly number of reports on the negative effects of photoactivated TiO2 to non-target organisms. We have here studied the effect of a suite of reference type TiO2 NMs i.e. NM103, NM104, NM105 and compared these to the Bulk) with and without UV radiation to the oligochaete Enchytraeus crypticus. High-throughput gene expression was used to assess the molecular mechanisms, while also anchoring it to known effects at organism level (i.e., reproduction). Results showed that the photoactivity of TiO2 (UV exposed) played a major role in enhancing TiO2 toxicity, activating transcription of oxidative stress, lysosome damage and apoptosis mechanisms. For non-UV activated TiO2, where toxicity at organism level (reproduction) was lower, results showed the potential for long-term effects (i.e., mutagenic and epigenetic). NM specific mechanisms were identified: NM103 affected transcription and translation, NM104_UV negatively affected reproductive system/organs; and NM105_UV activated superoxide anion response. Results provided mechanistic information for UV-related phototoxicity of TiO2 materials and evidences of the potential long-term effects.
2018-11-07 | GSE81699 | GEO
Project description:Epidermal melanocytes form synaptic-like contacts with cutaneous nerve fibers but the functional outcome of this connection remains elusive. In this pilot study, we used our fully humanized re-innervated skin organ culture model to investigate whether melanocyte-nerve fibers interaction play a role in UV-B-induced melanogenesis. UV-B-irradiation significantly enhanced melanin content and tyrosinase activity in re-innervated skin ex vivo compared to non-innervated controls, indicating that neuronal presence is essential for exacerbating pigmentation upon UV-B irradiation in long-term culture. Comparative transcriptomic analysis between laser-capture-microdissected melanocytes from freshly embedded human skin and published microarray data on in vitro primary melanocytes identified Semaphorin-4A (SEMA4A) as possible mediator of melanocyte-nerve fibers interactions. SEMA4A protein levels in Gp100+ epidermal melanocytes were significantly higher in re-innervated skin than in skin alone, and reduced by UV-B treatment. Analysis of melanocytes in vitro showed reduced SEMA4A protein expression 24h after UV-B-irradiation while SEMA4A secretion into the medium was increased. In sensory neurons, conditioned media (CM) from UV-B irradiated melanocytes stimulated tubulin expression and axon growth. Re-transfer of CM from neurons that received CM from melanocytes back to melanocytes resulted into significant increased melanin content only when the CM derived from neurons previously receiving CM from UV-B irradiated melanocytes. These findings highlight the importance of melanocyte-neuron interactions for UV-B-induced melanogenesis and suggest that secreted proteins (e.g. SEMA4A) can function as a novel target in the treatment of hypo- and hyperpigmentation disorders.
2024-12-31 | GSE271182 | GEO
Project description:To investigate the mechanistic effects of UV irradiation on pea seedlings at the protein level, proteomic analyses were performed on pea seedlings irradiated daily with 0 and 10 min UV-B.
2023-05-04 | PXD038486 | Pride
Project description:Purpose: Light is one of the most important environmental signal that affects the physiology and action of Volvox carteri. However, there are limited reports about the effects of UV-B irradiation on genome-wide transcriptional regulation in this organism. We surveyed the overall transcriptional responses of somatic and reproductive cells to UV-B irradiation using RNA-seq data. Methods: The somatic and reproductive cells were separated. The cell-types were treated for one hour by low-doses UV-B irradiation. Three biological replicates per cell-types (totally 12 samples) were used for RNA extraction. High-throughput RNA sequencing performed with separated-cells samples. Sequencing runs were performed on an Illumina HiSeq-2500. Transcriptome analysis was carried out in order to elucidate the effect of UV-B irradiation on whole transcriptional modification of physiological mechanisms. Results: In total, 264 and 272 million clean reads were produced in somatic and reproductive cells, respectively. The results showed that, as compared to control group, there were no differentially expressed genes in reproductive cells under treatment. However, treating the somatic cells with UV-B irradiation resulted in 126 differential genes as compared to untreated control group. Our results showed that there is light-specific transcriptional regulation in this organism. So that, different pathways were co-regulated by UV-B irradiation via the transcriptional regulation of genes encoding key enzymes in these pathways. Conclusions: Our findings showed that low UV-B irradiation influence on the cell-type specific gene expression. The findings of this study may present new insights to understand responsive mechanisms to UV-B irradiation by modulating expression of cell-type specific in the V. carteri.
2020-04-10 | GSE124346 | GEO
Project description:Cockayne syndrome B (CSB) protein is a member of the SWI/SNF family and has DNA-dependent ATPase and ATP-dependent chromatin remodeling activities. The CSB protein is missing or altered in CS-B cells. CS-B cells are hypersensitive to UV light and defective in transcription-coupled DNA repair (TCR). TCR efficiently removes a variety of lesions from the transcribed strand of active genes. It has been shown that lesions specifically in the transcribed strand of active genes trigger the induction of apoptosis following UV irradiation. Several DNA damage signaling cascades, including the ATR/Chk1, p38 kinase, p53, and jun N-terminal kinase pathways are activated following UV irradiation. However, the role of TCR in cellular global transcriptional responses to UV irradiation remains to be elucidated. Using oligonucleotide microarray technology, we analyzed the time course of responses of CS-B cells (CS-B) and CS-B cells complemented with wild-type CSB cDNA (CS-B wt). Experiment Overall Design: In order to investigate the global transcriptional responses to UV damage in TCR-proficient or TCR-deficient cells, CS-B wt and CS-B cells were irradiated with 10 J/m2 of UV light and incubated for 2 or 12 hours. All experiments were performed in triplicate.
2008-06-17 | E-GEOD-8939 | biostudies-arrayexpress
Project description:Somatic mutations are highly enriched at transcription factor (TF) binding sites, with the strongest trend being observed for ultraviolet light (UV)-induced mutations in melanomas. One of the main mechanisms proposed for this hyper-mutation pattern is the inefficient repair of UV lesions within TF-binding sites, caused by competition between TFs bound to these lesions and the DNA repair proteins that must recognize the lesions to initiate repair. However, TF binding to UV-irradiated DNA is poorly characterized, and it is unclear whether TFs maintain specificity for their DNA sites after UV exposure. We developed UV-Bind, a high-throughput approach to investigate the impact of UV irradiation on protein-DNA binding specificity. We applied UV-Bind to ten TFs from eight structural families, and found that UV lesions significantly altered the DNA-binding preferences of all TFs tested. The main effect was a decrease in binding specificity, but the precise effects and their magnitude differ across factors. Importantly, we found that despite the overall reduction in DNA-binding specificity in the presence of UV lesions, TFs can still compete with repair proteins for lesion recognition, in a manner consistent with their specificity for UV-irradiated DNA. In addition, for a subset of TFs we identified a surprising but reproducible effect at certain non-consensus DNA sequences, where UV irradiation leads to a high increase in the level of TF binding. These changes in DNA-binding specificity after UV irradiation, at both consensus and non-consensus sites, have important implications for the regulatory and mutagenic roles of TFs in the cell.
2023-01-20 | GSE223012 | GEO
Project description:Somatic mutations are highly enriched at transcription factor (TF) binding sites, with the strongest trend being observed for ultraviolet light (UV)-induced mutations in melanomas. One of the main mechanisms proposed for this hyper-mutation pattern is the inefficient repair of UV lesions within TF-binding sites, caused by competition between TFs bound to these lesions and the DNA repair proteins that must recognize the lesions to initiate repair. However, TF binding to UV-irradiated DNA is poorly characterized, and it is unclear whether TFs maintain specificity for their DNA sites after UV exposure. We developed UV-Bind, a high-throughput approach to investigate the impact of UV irradiation on protein-DNA binding specificity. We applied UV-Bind to ten TFs from eight structural families, and found that UV lesions significantly altered the DNA-binding preferences of all TFs tested. The main effect was a decrease in binding specificity, but the precise effects and their magnitude differ across factors. Importantly, we found that despite the overall reduction in DNA-binding specificity in the presence of UV lesions, TFs can still compete with repair proteins for lesion recognition, in a manner consistent with their specificity for UV-irradiated DNA. In addition, for a subset of TFs we identified a surprising but reproducible effect at certain non-consensus DNA sequences, where UV irradiation leads to a high increase in the level of TF binding. These changes in DNA-binding specificity after UV irradiation, at both consensus and non-consensus sites, have important implications for the regulatory and mutagenic roles of TFs in the cell.
2023-01-20 | GSE223022 | GEO
Project description:Somatic mutations are highly enriched at transcription factor (TF) binding sites, with the strongest trend being observed for ultraviolet light (UV)-induced mutations in melanomas. One of the main mechanisms proposed for this hyper-mutation pattern is the inefficient repair of UV lesions within TF-binding sites, caused by competition between TFs bound to these lesions and the DNA repair proteins that must recognize the lesions to initiate repair. However, TF binding to UV-irradiated DNA is poorly characterized, and it is unclear whether TFs maintain specificity for their DNA sites after UV exposure. We developed UV-Bind, a high-throughput approach to investigate the impact of UV irradiation on protein-DNA binding specificity. We applied UV-Bind to ten TFs from eight structural families, and found that UV lesions significantly altered the DNA-binding preferences of all TFs tested. The main effect was a decrease in binding specificity, but the precise effects and their magnitude differ across factors. Importantly, we found that despite the overall reduction in DNA-binding specificity in the presence of UV lesions, TFs can still compete with repair proteins for lesion recognition, in a manner consistent with their specificity for UV-irradiated DNA. In addition, for a subset of TFs we identified a surprising but reproducible effect at certain non-consensus DNA sequences, where UV irradiation leads to a high increase in the level of TF binding. These changes in DNA-binding specificity after UV irradiation, at both consensus and non-consensus sites, have important implications for the regulatory and mutagenic roles of TFs in the cell.
2023-01-20 | GSE223021 | GEO