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1,335 results for “Oxidative stress.”
An orphan LuxR homolog of Bradyrhizobium japonicum is important for oxidative stress tolerance and competitiveness during soybean nodulation
GEO Series GSE22389. Bradyrhizobium japonicum; Bradyrhizobium diazoefficiens USDA 110. 20 samples. Type: Expression profiling by array.
Calreticulin Ins5 and Del52 mutations impair unfolded protein and oxidative stress responses in hematopoietic cells
GEO Series GSE102900. Homo sapiens. 9 samples. Type: Expression profiling by array.
A chromatin-driven mechanism of transcription in ammonia-oxidizing archaea under environmental stress
GEO Series GSE249033. Nitrososphaera viennensis EN76. 6 samples. Type: Expression profiling by high throughput sequencing; Genome binding/occupancy profiling by high throughput sequencing.
Loss of beta-catenin triggers oxidative stress and impairs hematopoietic regeneration
GEO Series GSE50620. Mus musculus. 6 samples. Type: Expression profiling by array.
Modulatory Role of Radioprotective 105 in Mitigating Oxidative Stress and Ferroptosis via the HO-1/SLC7A11/GPX4 Axis in Sepsis-mediated renal injury
GEO Series GSE294514. Mus musculus. 6 samples. Type: Expression profiling by high throughput sequencing.
Beta vulgaris-Derived Exosome-like Nanovesicles Mitigate Photoaging by Attenuating Oxidative Stress and Promoting Collagen Biosynthesis Abstract
GEO Series GSE310833. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Alteration of hepatic gene expression profile in NPC mice correlates with tissue damage and oxidative stress status
GEO Series GSE24013. Mus musculus. 3 samples. Type: Expression profiling by array.
Protein acyltransferase DHHC3 regulates breast tumor growth, oxidative stress and senescence.
GEO Series GSE102776. Homo sapiens; Mus musculus. 4 samples. Type: Expression profiling by array.
Expression profiles of Pseudomonas aeruginosa TBCF10839 wild type and nadk1 mutant under oxidative stress conditions
GEO Series GSE21704. Pseudomonas aeruginosa. 10 samples. Type: Expression profiling by array.
The bZIP transcription factor Atf1 governs the oxidative stress response and sexual differentiation of Cryptococcus neoformans downstream of the HOG pathway
GEO Series GSE64871. Cryptococcus neoformans; Cryptococcus deneoformans JEC21. 11 samples. Type: Expression profiling by array.
The Histone Methyltransferase Setd2 Modulates Oxidative Stress to Attenuates Colonic Inflammation and Tumorigenesis [ChIP-Seq]
GEO Series GSE151965. Mus musculus. 4 samples. Type: Genome binding/occupancy profiling by high throughput sequencing.
MiR-204-5p may Regulate Oxidative Stress in Myopia and Myopia-Related Retinopathy
GEO Series GSE253960. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
Activation of FXR regulates oxidative stress responses in human keratinocytes.
GEO Series GSE305364. Homo sapiens. 9 samples. Type: Expression profiling by high throughput sequencing.
Dataset related to the article "Impact of oxidative stress and protein S-Glutathionylation in aortic valve sclerosis patients with overt atherosclerosis
<p>This record contains raw data related to the article "Impact of oxidative stress and protein S-Glutathionylation in aortic valve sclerosis patients with overt atherosclerosis"</p> <p>Abstract: Aortic valve sclerosis (AVSc) is characterized by non-uniform thickening of the leaflets without hemodynamic changes. Endothelial dysfunction, also caused by dysregulation of glutathione homeostasis expressed as ratio between its reduced (GSH) and its oxidised form (GSSG), could represent one of the pathogenic triggers of AVSc. We prospectively enrolled 58 patients with overt atherosclerosis and requiring coronary artery bypass grafting (CABG). The incidence of AVSc in the studied population was 50%. The two groups (No-AVSc and AVSc) had similar clinical characteristics. Pre-operatively, AVSc group showed significantly lower GSH/GSSG ratio than No-AVSc group (<em>p</em> = 0.02). Asymmetric dimethylarginine (ADMA) concentration was significantly higher in AVSc patients compared to No-AVSc patients (<em>p</em> < 0.0001). Explanted sclerotic aortic valves presented a significantly increased protein glutathionylation (Pr-SSG) than No-AVSc ones (<em>p</em> = 0.01). In vitro, inhibition of glutathione reductase caused β-actin glutathionylation, activation of histone 2AX, upregulation of α2 smooth muscle actin (<em>ACTA2</em>), downregulation of platelet and endothelial cell adhesion molecule 1 (<em>PECAM1</em>) and cadherin 5 (<em>CDH5</em>). In this study, we showed for the first time that the dysregulation of glutathione homeostasis is associated with AVSc. We found that Pr-SSG is increased in AVSc leaflets and it could lead to EndMT via DNA damage. Further studies are warranted to elucidate the causal role of Pr-SSG in aortic valve degeneration</p>
Data set from the article Massaccesi L, Galliera E, Galimberti D, Fenoglio C, Arcaro M, Goi G, Barassi A, Corsi Romanelli MM. Lag-time in Alzheimer's disease patients: a potential plasmatic oxidative stress marker associated with ApoE4 isoform. Immun Ageing. 2019 Apr 1;16:7. doi: 10.1186/s12979-019-0147-x. PMID: 30984280; PMCID: PMC6444862.
<p>Data set from the article: Massaccesi L, Galliera E, Galimberti D, Fenoglio C, Arcaro M, Goi G, Barassi A, Corsi Romanelli MM. Lag-time in Alzheimer's disease patients: a potential plasmatic oxidative stress marker associated with ApoE4 isoform. Immun Ageing. 2019 Apr 1;16:7. doi: 10.1186/s12979-019-0147-x. PMID: 30984280; PMCID: PMC6444862.</p> <p>This is the astract:</p> <p>In the brain, Oxidative Stress (OS) contribute to structural and functional changes associated with vascular aging, such as endothelial dysfunction, extracellular matrix degradation, resulting in age-related reduced vasodilatation in response to agonists. For this reason, OS is considered a key factor in Alzheimer's Disease (AD) development and recent evidence correlated oxidative stress with vascular lesion in the pathogenesis of AD, but the mechanism still need to be fully clarified. The etiology of AD is still not completely understood and is influenced by several factors including Apolipoprotein E (ApoE) genotype. In particular, the Apo ε4 isoform is considered a risk factor for AD development. This study was aimed to evaluate the possible relationship between three plasmatic OS marker and Apo ε4 carrier status. Plasmatic soluble receptor for advanced glycation end products (sRAGE) levels, plasma antioxidant total defenses (by lag-time method) and plasmatic Reactive Oxygen species (ROS) levels were evaluated in 25 AD patients and in 30 matched controls. ROS were significantly higher while plasma antioxidant total defenses and sRAGE levels were significantly lower in AD patients compared to controls. In AD patients lag-time values show a significant positive linear correlation with sRAGE levels and a (even not significant) negative correlation with ROS levels. Lag-time is significantly lower in ε4 carrier (<em>N</em> = 13) than in ε4 non-carrier (<em>N</em> = 12). Our result confirms the substantial OS in AD. Lag-time levels showed a significant positive correlation with sRAGE levels and a significant association with ε4 carrier status suggesting that plasmatic lag-time evaluation can be considered as a potential useful OS risk marker in AD.</p> <p> </p>
Impact of Crowding on Autophagy and Oxidative Stress in Rainbow Trout
<p>Supplementary tables of publication</p>
HuD regulates SOD1 expression during oxidative stress in differentiated neuroblastoma cells and sporadic ALS motor cortex
<p><strong>The database includes </strong>the raw of the article “HuD regulates SOD1 expression during oxidative stress in differentiated neuroblastoma cells and sporadic ALS motor cortex”.</p> <p><strong>In detail, the database contains</strong> data obtained by the following evaluations: i) RNA electrophoretic mobility shift assay (REMSA) to detect the formation of a complex between HuD recombinant protein and SOD1 ARE sequences. ii) multiplex qRT-PCR to evaluate if oxidative stress levels, i.e H2O2 treatment, induces a shift in the alternative polyadenylation (APA) site usage in SOD1 3'UTR.</p> <p><strong>Aim of the work</strong> was to investigate the potential involvement of HuD (ELAVL4) one of the neuronal members of the ELAVL family, in SOD1 regulation during oxidative stress and in sporadic ALS patients (sALS).</p> <p>Using differentiated SH-SY5Y cells along with brain tissues from sALS patients, we evaluated HuD-dependent regulation of SOD1 mRNA. By means in vitro binding and mRNA decay assays we observed that HuD specifically binds to SOD1 ARE motifs promoting mRNA stabilization. In SH-SY5Y cells, we faound that the overexpression of full-length HuD increased SOD1 mRNA and protein levels; moreover HuD regulation of SOD1 mRNA we found that this regulation is related to oxidative stress, as shown after H2O2 exposure. H2O2 exposure also induced a shift in the APA site usage in SOD1 3'UTR, increasing the levels of a long variant bearing HuD binding sites. We validated this data using a specific siRNA. In the motor cortex from sALS patients, we found increases in SOD1 and HuD mRNAs and proteins, accompanied by greater HuD binding to this mRNA as confirmed by RNA-immunoprecipitation (RIP) assays.</p> <p><strong>To conclude,</strong> these results point a role of HuD in the post-transcriptional regulation of SOD1 expression in neurons after oxidative stress and in sALS brain tissues, thus suggesting an involvement in ALS pathogenesis.</p>
Dataset relate to the article "Oxidative Stress and Arginine/Nitric Oxide Pathway in Red Blood Cells Derived from Patients with Prediabetes"
<p>This record contains row data relaed to the article "Oxidative Stress and Arginine/Nitric Oxide Pathway in Red Blood Cells Derived from Patients with Prediabetes"</p> <p><strong>Abstract: </strong>The effects of the oral glucose tolerance test (OGTT) on red blood cells (RBCs) have not been thoroughly investigated, although it is known that the<strong> </strong>ingestion of<strong> </strong>75-g<strong> </strong>glucose during OGTT results in a systemic state of inflammation and oxidative stress. Therefore, we evaluated the effect of OGTT on oxidative stress and L-Arginine/Nitric Oxide (L-Arg/NO) metabolic pathway in RBCs obtained from patients with prediabetes. Blood samples were collected from all participants before (T0) and at 10 (T1), 20 (T2), 30 (T3), 60 (T4), 90 (T5), 120 (T6), 150 (T7), and 180 (T8) minutes after glucose loading. Results showed a significant increase in oxidative stress status characterized by a rise in the GSSG/GSH ratio at T4 and T6 that went in parallel with a reduction of NO production in RBCs. In addition, in this time frame, increased exposure of phosphatidylserine on RBCs membrane was observed. These metabolic modifications were rescued at T8, together with an increase in activated RBC NO synthase expression.<strong> T</strong>hese findings provide a possible explanation of the phenomena occurring after glucose loading and suggest that, even in the early stages of diabetes, it may be important to avoid acute variations in glycemia in order to prevent diabetic complications.</p>
Metformin treatment reduces oxidative stress state of RNASEH2-mutated Aicardi-Goutières patients-derived Lymphoblastoid Cell Lines
<p>The database includes the raw data of the article “Metformin treatment reduces oxidative stress state of RNASEH2-mutated Aicardi-Goutières patients-derived Lymphoblastoid Cell Lines”. Aim of this work was was to examine the impact of metformin treatment on the oxidative stress state of lymphoblastoid cell lines (LCLs) carrying mutation in RNASEH2B and RNASEH2A AGS related genes and healthy control. The database contains the data obtained by the following evaluations: a) Flow cytometry analysis for the evaluation of ROS release; b) Immunofluorescence for the evaluation of the stress-induced DNA damage by the quantification of the 8-OxoG level and changes of altered membrane potential by the quantification of monomeric and aggregated JC-1 dye; c) RT-qPCR for the evaluation of the expression level of FOXO3-related pathway.</p> <p>We demonstrated that metformin is able to highly reduce ROS overproduction especially in RNASEH2B-mutated LCLs, to restore the impaired mitochondrial membrane potential and strongly reduce the oxidative DNA damage by reducing the 8-oxoG level in AGS patients. We demonstrated that the beneficial effect of metformin associate with the upregulation of FOXO3-related signaling pathway. Metformin treatment seem to represents a possible therapeutic approach, useful to ameliorate the oxidative stress-related inflammatory condition observed in AGS subjects.</p>
Del Nido Cardioplegia or Potassium Induces Nrf2 and Protects Cardiomyocytes Against Oxidative Stress
GEO Series GSE221058. Homo sapiens. 6 samples. Type: Expression profiling by high throughput sequencing.
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Allen Brain Atlas
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Annotated Behaviour and Observability Dataset (ABODe)
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