Homo sapiens
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ABSTRACT:
PROVIDER: PRJNA128595 | ENA |
REPOSITORIES: ENA
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Project description:Oxidative exposure of cells occurs naturally and may be associated with cellular damage and dysfunction. Protracted low level oxidative exposure can induce accumulated cell disruption, affecting multiple cellular functions. Accumulated oxidative exposure has also been proposed as one of the potential hallmarks of the physiological/pathophysiological aging process. We investigated the multifactorial effects of long-term minimal peroxide exposure upon SH-SY5Y neural cells to understand how they respond to the continued presence of oxidative stressors. We show that minimal protracted oxidative stresses induce complex molecular and physiological alterations in cell functionality. Upon chronic exposure to minimal doses of hydrogen peroxide, SH-SY5Y cells displayed a multifactorial response to the stressor. To fully appreciate the peroxide-mediated cellular effects, we assessed these adaptive effects at the genomic, proteomic and cellular signal processing level. Combined analyses of these multiple levels of investigation revealed a complex cellular adaptive response to the protracted peroxide exposure. This adaptive response involved changes in cytoskeletal structure, energy metabolic shifts towards glycolysis and selective alterations in transmembrane receptor activity. Our analyses of the global responses to chronic stressor exposure, at multiple biological levels, revealed a viable neural phenotype in-part reminiscent of aged or damaged neural tissue. Our paradigm indicates how cellular physiology can subtly change in different contexts and potentially aid the appreciation of stress response adaptations.
2012-09-20 | GSE22525 | GEO
Project description:The Y79 retinoblastoma cells were exposed to oxidative stress conditions with hydrogen peroxide exposure. The differential gene expression profile on this condition was evaluated by comparing with untreated control Y79 cells. The cellular responses based on the differential gene expression was studied.
2011-03-11 | GSE27880 | GEO
Project description:Bacillus subtilis exhibits a complex adaptive response to low levels of peroxides. We used global transcriptional profiling to monitor the magnitude and kinetics of changes in the mRNA population after exposure to either hydrogen peroxide (H2O2) or tert-butyl peroxide (t-buOOH). The peroxide stimulons could be largely accounted for by three regulons controlled by the PerR, B, and OhrR transcription factors. Three members of the PerR regulon (katA, mrgA, and zosA) were strongly induced by H2O2 and weakly induced by t-buOOH. The remaining members of the PerR regulon were only modestly up-regulated by peroxide treatment. Overall, the magnitude of peroxide induction of PerR regulon genes corresponded well with the extent of derepression in a perR mutant strain. The B regulon was activated by 58 µM H2O2 but not by 8 µM H2O2 and was strongly activated by either t-buOOH or, in a control experiment, tert-butyl alcohol. Apart from the B regulon there was a single gene, ohrA, that was strongly and rapidly induced by t-buOOH exposure. This gene, controlled by the peroxide-sensing repressor OhrR, was not induced by any of the other conditions tested. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Computed
2005-08-16 | E-GEOD-3138 | biostudies-arrayexpress
Project description:Bacillus subtilis exhibits a complex adaptive response to low levels of peroxides. We used global transcriptional profiling to monitor the magnitude and kinetics of changes in the mRNA population after exposure to either hydrogen peroxide (H2O2) or tert-butyl peroxide (t-buOOH). The peroxide stimulons could be largely accounted for by three regulons controlled by the PerR, B, and OhrR transcription factors. Three members of the PerR regulon (katA, mrgA, and zosA) were strongly induced by H2O2 and weakly induced by t-buOOH. The remaining members of the PerR regulon were only modestly up-regulated by peroxide treatment. Overall, the magnitude of peroxide induction of PerR regulon genes corresponded well with the extent of derepression in a perR mutant strain. The B regulon was activated by 58 µM H2O2 but not by 8 µM H2O2 and was strongly activated by either t-buOOH or, in a control experiment, tert-butyl alcohol. Apart from the B regulon there was a single gene, ohrA, that was strongly and rapidly induced by t-buOOH exposure. This gene, controlled by the peroxide-sensing repressor OhrR, was not induced by any of the other conditions tested. Set of arrays organized by shared biological context, such as organism, tumors types, processes, etc. Keywords: Logical Set
2005-08-16 | GSE3138 | GEO
Project description:A transcriptionally induced antioxidant program is elicited in thyroid cells after exposure to hydrogen peroxide
| PRJNA170114 | ENA
Project description:CD4 T cells play critical roles in promoting inflammation and helping immune responses, but knowledge of how memory CD4 T cells are regulated and how they help adaptive immune responses is limited. Using adoptive transfer of virus-specific CD4 T cells, we show that naïve CD4 T cells undergo substantial expansion following viral infection, but can induce lethal TH1-driven inflammation. In contrast, memory CD4 T cells exhibit a biased proliferation of T follicular helper (Tfh) cell subsets that correlate with improved adaptive responses and minimal tissue damage following viral infection. Importantly, our analyses revealed that type I interferon regulates the expansion of naïve CD4 T cells, but does not seem to play a critical role in regulating the expansion of memory CD4 T cells. Moreover, blockade of type I interferon signaling abrogated lethal CD4 T cell inflammation following viral infection. Taken together, these data demonstrate a previously undescribed function for memory CD4 T cells: to help adaptive immunity with minimal harm to the host. These findings are important for rational vaccine design and for improving the safety and efficacy of adoptive T cell therapies against persistent antigens. Primary and memory SMARTA cells were MACS-purified by negative selection (STEMCELL) and then FACS-sorted to 98% purity on a FACS Aria (BD Biosciences) according to congenic marker expression (CD45.1+ for secondary, and CD45.1+ CD45.2+ for primary, CD4 T cell responses).
2017-03-31 | GSE92474 | GEO
Project description:The Y79 retinoblastoma cells were exposed to oxidative stress conditions with hydrogen peroxide exposure. The differential gene expression profile on this condition was evaluated by comparing with untreated control Y79 cells. The cellular responses based on the differential gene expression was studied. One-color experiment,Organism: Human , Custom Whole Genome Human 8x60k designed by Genotypic Technology Pvt. Ltd. (Agilent-27114), Labeling kit: Agilent Quick-Amp labeling Kit (p/n5190-0442)
2011-03-11 | E-GEOD-27880 | biostudies-arrayexpress
Project description:Oxidative stress, resulting from an imbalance in the accumulation and removal of reactive oxygen species such as hydrogen peroxide (H2O2), is a challenge faced by all aerobic organisms. In plants, exposure to various abiotic and biotic stresses results in accumulation of H2O2 and oxidative stress. Increasing evidence indicates that H2O2 functions as a stress signal in plants, mediating adaptive responses to various stresses. To analyze cellular responses to H2O2, we have undertaken a large-scale analysis of the Arabidopsis transcriptome during oxidative stress. Using cDNA microarray technology, we identified 175 non-redundant expressed sequence tags that are regulated by H2O2. Of these, 113 are induced and 62 are repressed by H2O2. A substantial proportion of these expressed sequence tags have predicted functions in cell rescue and defense processes. RNA-blot analyses of selected genes were used to verify the microarray data and extend them to demonstrate that other stresses such as wilting, UV irradiation, and elicitor challenge also induce the expression of many of these genes, both independently of, and, in some cases, via H2O2. replicate_design
2012-07-23 | E-GEOD-39570 | biostudies-arrayexpress
Project description:Oxidative stress, resulting from an imbalance in the accumulation and removal of reactive oxygen species such as hydrogen peroxide (H2O2), is a challenge faced by all aerobic organisms. In plants, exposure to various abiotic and biotic stresses results in accumulation of H2O2 and oxidative stress. Increasing evidence indicates that H2O2 functions as a stress signal in plants, mediating adaptive responses to various stresses. To analyze cellular responses to H2O2, we have undertaken a large-scale analysis of the Arabidopsis transcriptome during oxidative stress. Using cDNA microarray technology, we identified 175 non-redundant expressed sequence tags that are regulated by H2O2. Of these, 113 are induced and 62 are repressed by H2O2. A substantial proportion of these expressed sequence tags have predicted functions in cell rescue and defense processes. RNA-blot analyses of selected genes were used to verify the microarray data and extend them to demonstrate that other stresses such as wilting, UV irradiation, and elicitor challenge also induce the expression of many of these genes, both independently of, and, in some cases, via H2O2
2007-05-04 | E-SMDB-4011 | biostudies-arrayexpress
Project description:Particulate matter 2.5 (PM2.5) deposition in the lung’s alveolar capillary region (ACR) is significantly associated with respiratory disease development, yet the underlying molecular mechanisms are not completely understood. Adverse responses that promote respiratory disease development involve orchestrated, intercellular signaling between multiple cell types within the ACR. Our goal was to use an organotypic, in vitro model of the ACR to investigate if alveolar epithelial PM2.5 exposure induces exposure responses in alveolar epithelial cells and in underlying microvascular endothelial cells in the ACR. Our findings demonstrate that alveolar epithelial PM2.5 exposure induces robust transcriptional responses in the microvascular endothelial cells within the ACR. We show that the underlying microvascular endothelial cells develop redox dysfunction and increase proinflammatory cytokine secretion, two exposure responses commonly associated with respiratory disease development. Moreover, we identified intercellular signaling mechanisms between the alveolar epithelium and microvascular endothelium that modulate these adverse endothelial exposure responses. Our findings illustrate a new mechanism of intercellular communication between cells of the ACR that significantly improves our understanding of respiratory disease development following pulmonary exposure to inhaled materials.
2024-12-01 | GSE229544 | GEO