Transcriptional changes in response to oxidative stress in combination with temperature extremes in rice
Ontology highlight
ABSTRACT:
ORGANISM(S): Oryza sativa Oryza sativa Indica Group
PROVIDER: GSE32704 | GEO | 2012/12/26
SECONDARY ACCESSION(S): PRJNA146999
REPOSITORIES: GEO
Similar Datasets
Project description:Genome wide expression profiles of 10-day-old seedlings in response to prior exposure with OS followed by heat stress or cold stress as well simultaneous exposure to OS along with HS/CS was done to study the transcriptional changes in response to combination of stresses. 10-day old rice seedlings were used for experiments. Transcript profiling was done in 10-day old rice seedling following oxidative Stress prior to High Temperature Stress (PO_HS) or Low Temperature Stress (PO_CS) and Oxidative Stress during High Temperature Stress (DO_HS)/ during Low temperature stress (DO_CS). Unstressed seedlings were used as control. For each condition, three biological replicates were processed in a similar manner for the microarray analysis.
2012-12-26 | E-GEOD-32704 | biostudies-arrayexpress
Project description:Drug abuse is a major concern with few therapeutic options. Heparan sulfate (HS) and chondroitin sulfate (CS) interact with a plethora of growth factors and their receptors, and have profound effects on cellular signaling. Thus, targeting these dynamic interactions represents a novel therapeutic modality. Our previous studies have indicated increased HS proteoglycan syndecan-3 and identified HS as a resilience factor for cocaine abuse. Here, we utilized mass spectrometry-based glycomics and proteomics to understand the effects of cocaine (C) and methamphetamine (M) on HS, CS, and proteins from two brain regions: lateral hypothalamus (LH) and striatum (ST) from mice. We observed significant differences in HS and CS total abundances and percent sulfate contents and reduction in CS 4-O-sulfation, and increase in CS 6-O-sulfation for drug-treated (C and M) vs. saline samples. The proteomics data revealed a number of aberrant proteins in drug-treated vs. saline samples, including MYPR, KCC2A, SYN2, TENR, CALX, ANXA7, HDGF, NCAN, and CSPG5, and oxidative phosphorylation among the top perturbed pathway. Taken together, our study shows for the first time the novel relationship of HS, CS, and associated proteins with the drug abuse, and shed light on, the underlying neurobiological mechanism of drug dependence and novel therapeutic options.
2024-09-04 | PXD038576 | Pride
Project description:This study investigated whether mitochondria-targeted peptide SS-31 played a protective role in cigarette smoke (CS)-induced airway inflammation and oxidative stress in mice. Mice were exposed to CS for 4 weeks to establish a CS-induced airway inflammation model, then treated with SS-31. Pathological changes and oxidative stress in lung tissue, inflammatory cell counts and pro-inflammatory cytokines in bronchoalveolar lavage fluid (BALF) were examined. RNA sequencing from lung tissue and western blotting were conducted to investigate mechanisms. SS-31 attenuated CS-induced inflammatory injury of the airway. Numbers of total cells, neutrophils, and macrophages and levels of tumor necrosis factor α, interleukin 6, and matrix metallopeptidase 9 in BALF were markedly reduced by SS-31. SS-31 attenuated CS-induced oxidative stress by decresing malondialdehyde and myeloperoxidase levels, and increasing superoxide dismutase activity. It also reversed the expression of mitochondrial fission protein and optic atrophy 1 protein, and reduced cytochrome c release into the cytosol. RNA sequencing revealed that SS-31 changed CS-induced expression profiles and enriched MAPK pathway, western blotting confirmed that SS-31 inhibited the CS-activated MAPK pathway. SS-31 alleviates CS-induced airway inflammation and oxidative stress, possibly via the regulation of mitochondrial function and MAKP pathway, SS-31 may be a novel drug for CS-induced airway disorders.
2020-12-25 | GSE163835 | GEO
Project description:Prenatal environmental exposures that have been shown to induce oxidative stress (OS) during pregnancy, such as smoking and alcohol consumption, are risk factors for the onset of schizophrenia and other neurodevelopmental disorders (NDDs). While the OS role in the etiology of neurodegenerative diseases is well known, its contribution to the genomic dysregulation associated with psychiatric disorders is less well defined. In this study we used SH-SY5Y cell line and applied RNA-sequencing to explore transcriptomic changes in response to OS before or during neural differentiation. We observed differential expression of many genes, most of which localised to the synapse and involved in neuronal differentiation. These genes were enriched in schizophrenia-associated signalling pathways, including PI3K/Akt, axon guidance, and signalling by retinoic acid. Interestingly, circulatory system development was affected by both treatments, which is concordant with observations of increased prevalence of cardiovascular disease in patients with NDDs. We also observed a very significant increase in the expression of immunity-related genes, supporting current hypotheses of immune system involvement in psychiatric disorders. These data suggest that early life exposure to OS has a disruptive influence on neuronal gene expression that may perturb normal differentiation and neurodevelopment, thereby contributing towards overall risk for developing psychiatric diseases.
2020-12-15 | GSE161860 | GEO
Project description:Oxidative stress (OS) results from genetic defects or stressful environmental challenges that cause unchecked production of reactive oxygen species (ROS). OS has been implicated in many diseases due to its wide ranging damage to nucleic acids, proteins and lipids. Using Halobacterium salinarum NRC-1, an extremophile that thrives under conditions of excessive OS, we have constructed a systems model for oxidative stress response (OSR) by integrating transcriptional changes induced by treatments with H2O2 and paraquat, functional associations inferred through comparative genomics, and de novo discovered cis-regulatory motifs. Together with phenotypic analysis of mutant strains this has revealed a multi-tiered OS management program to transcriptionally coordinate three peroxidase/catalase enzymes, two superoxide dismutases, production of rhodopsins, carotenoids, and gas vesicles, metal trafficking, and various other aspects of metabolism. Remarkably, a significant fraction of this OSR was accurately recapitulated by a model that was previously constructed from cellular responses to diverse environmental perturbations –this constitutes the general stress response component. Notwithstanding this observation, comparison of the two models has identified the coordination of frontline defense and repair systems by regulatory mechanisms that are triggered uniquely by severe OS and not by other environmental stressors, including sub-inhibitory levels of redox-active metals, extreme changes in oxygen tension, and a sub-lethal dose of g rays.
2010-05-26 | GSE17515 | GEO
Project description:Effective therapies for metastatic osteosarcoma (OS) remain a major clinical unmet need. Targeting mRNA translation in metastatic OS represents an attractive option, as selective translation under stress supports the rapid synthesis of cytoprotective proteins that facilitate metastatic competence. We therefore assessed eukaryotic translation factors in OS, revealing high expression of eIF4A1 in metastatic OS. The eIF4A1 inhibitor, CR-1-31B, potently inhibited metastatic OS growth in vitro and reduced lung tumor burden in orthotopic mouse models. CR-1-31B synergized with the oxidative stress inducer, tert-butylhydroquinone (tBHQ), to enhance cell death under oxidative stress. Proteomic analysis revealed a subset of proteins that were upregulated by tBHQ alone, but inhibited by co-treatment of CR-1-31B, most notably the NRF2 antioxidant transcription factor, and NRF2 inactivation phenocopied CR-1-31B in blocking OS lung metastasis in vivo. Collectively, our data reveal that targeting eIF4A1 with CR-1-31B is highly effective in blocking OS metastasis by blunting the NRF2 antioxidant response.
2024-07-16 | PXD047420 | Pride
Project description:Proteoglycans (PGs) are proteins with glycosaminoglycan (GAG) chains, such as chondroitin sulfate (CS) or heparan sulfate (HS), attached to serine residues. We have earlier shown that prohormones can carry CS, thus, constituting a novel class of PGs. The mapping of GAG modifications of proteins in endocrine cells may thus assist us in delineating possible roles of PGs in endocrine cellular physiology. With this aim, we applied a glycoproteomic approach to identify PGs, their GAG chains and their attachment sites in insulin-secreting cells. Glycopeptides carrying GAG chains were enriched from human pancreatic islets, rat (INS-1 832/13) and mouse (MIN6, NIT-1) insulinoma cell lines by ion exchange chromatography, depolymerized with GAG lyases, and analyzed by nanoflow liquid chromatography-tandem mass spectrometry (nLC-MS/MS). We identified CS modifications of chromogranin-A, islet amyloid polypeptide, secretogranin 1 and secretogranin 2, immunoglobulin superfamily member 10, and protein AMBP. Additionally, we identified two HS-modified prohormones (chromogranin-A and secretogranin-1), which was surprising, as prohormones are not typically regarded as HSPGs. For chromogranin-A, the glycosylation site carried either CS or HS, making it a so-called hybrid site. Additional HS sites were found on syndecan-1, syndecan-4, nerurexin-2, protein NDNF, and testican-1. These results demonstrate that several prohormones, and other constituents of the insulin-secreting cells are PGs. Cell-targeted mapping of the GAG glycoproteome forms an important basis for better understanding of endocrine cellular physiology, and the novel CS and HS sites presented here provide important knowledge for future studies.
2022-02-16 | PXD024230 | Pride
Project description:Worsening temperature extremes are among the most severe impacts of human-induced climate change. These extremes are often defined as rare events that exceed a specific percentile threshold within the distribution of daily maximum temperature. The percentile-based approach is chosen to follow regional and seasonal temperature variations so that extremes can occur globally and in all seasons, and frequently uses a running seasonal window to increase the sample size for the threshold calculation. Here, we show that running seasonal windows as used in many studies in recent years introduce a time-, region-, and dataset-depended bias that can lead to a striking underestimation of the expected extreme frequency. We reveal that this bias arises from artificially mixing the mean seasonal cycle into the extreme threshold and propose a simple solution that essentially eliminates it. We then use the corrected extreme frequency as reference to show that the bias also leads to an overestimation of future heatwave changes by as much as 30% in some regions. Based on these results we stress that running seasonal windows should not be used without correction for estimating extremes and their impacts.
| S-EPMC10948863 | biostudies-literature
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress. Chromatin immunoprecipitation coupled sequencing of 2 histone modifications in BJ (hTert/sT) and total levels of RNA polymerase II after 0, 30 and 120 minutes of treatment with H2O2 in MRC5 cells.
2015-05-27 | E-GEOD-55171 | biostudies-arrayexpress
Project description:Oxidative stress (OS) is caused by an imbalance between pro-oxidant and antioxidant reactions which leads to accumulation of reactive oxygen species (ROS) within cells. ROS can be harmful, due to their damaging effects on several cellular components, but are at the same time essential components of signaling cues. We investigate the effect of OS on the immediate early transcriptional response at a genomic level, by deep sequencing of nuclear and cytosolic RNA fractions, in in human fibroblasts treated for 30 or 120 minutes with sub-lethal doses of H2O2. In contrast to most of the protein-coding transcriptome, OS induces de novo transient transcription of thousands of previously uncharacterized genomic loci. We classify these stress induced long non coding RNAs (lncRNA) based on their genomic annotation and strand orientation relative to their nearest gene: distal, overlapping, terminal-associated or promoter-associated. The latter class of stress-induced promoter associated antisense lncRNAs (si-paancRNAs), is preferentially transcribed by PolII, which elongates from bidirectional promoters, enriched for specific transcription factor-binding sites (ZFP161, ZFX, MEF2A and divergent-FOS motives). Interestingly the associated sense-coding genes belong to specific functional categories (cellular response to stress and others). We finally demonstrate that a subset of si-paancRNAs associate better with the translation machinery, which is stalled, upon OS. Most studies to date have focused on the repertoire of lncRNAs present in physiological conditions. We here report the surprising result that thousands of lncRNAs are transcriptionally upregulated upon OS from specific loci possibly playing a role in physiological or pathological response to stress. RNA-Sequencing profiles of nuclear and cytosolic fractions of fibroblast cell lines after 0, 30 and 120 minutes of treatment with H2O2.
2015-05-27 | E-GEOD-55169 | biostudies-arrayexpress