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984 results for “Cell stress”
Data from: Use of a microfluidic platform to uncover basic features of energy and environmental stress responses in individual cells of Bacillus subtilis
Bacteria use a variety of stress-sensing systems to sense and respond to diverse stressors and to ensure their survival under adverse conditions. The gram-positive bacterium Bacillus subtilis responds to energy stress (ATP depletion) and to environmental stressors using two distinct stress-sensing pathways that converge on the alternative sigma factor σB to provoke a general stress response. Past efforts to study the σB stress response in bulk culture and on agarose pads were unable to visualize the responses of individual cells under tightly controlled conditions for extended periods of time. Here we use a microfluidics-based strategy to discern the basic features of σB activation in single cells in response to energy and environmental stress, both immediately upon stressor exposure and for tens of generations thereafter. Upon energy stress at various levels of stressor, cells exhibited fast, transient, and amplitude-modulated responses but not frequency modulation as previously reported. Upon environmental stress, which is mediated by the stressosome complex, wild-type cells primarily exhibited a transient and amplitude-modulated response. However, mutant cells producing only one of the four paralogous RsbR stressosome proteins showed striking and previously unseen differences. Whereas RsbRA-only cells mimicked the wild type, RsbRC-only cells displayed a slower but sustained overall response composed of repeated activation events in single cells.
Figure 2 from: Kokanova-Nedialkova Z, Aluani D, Tzankova V, Nedialkov P (2021) Simultaneous quantification of the major flavonoids from wild spinach by UHPLC-HRMS and their neuroprotective effects in a model of H2O2-induced oxidative stress on SH-SY5Y cells. Pharmacia 68(3): 657-664. https://doi.org/10.3897/pharmacia.68.e71030
Figure 2 Effect of flavonoids and silibinin on the viability of neuroblastoma SH-SY5Y cells. Data are presented as means from three independent experiments ± SD (n = 8). *P < 0.05, ***P < 0.001, vs. untreated control (one-way analysis of variance with Dunnet's post hoc test).
Figure 5 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654
Figure 5 Compound 5 induces the ER-mediated apoptosis. A) Representative Western blot showing the enhanced release of Smac/DIABLO but not cytochrome c from the mitochondria (MF) into the cytosol (CF) of compound 5-treated A549 lung cancer cells (GI50). Equal protein loading was controlled by staining membranes with Ponceau S (a representative section of the stained membrane is shown). The experiment was repeated three times and the corresponding quantification is shown in (B), B) Quantification of smac/DIABLO and cytochrome C levels in vehicle-treated control A549 cells and cells treated with GI50 amount of compound 5 or 5% DMSO as a negative control. M: mitochondria fraction; C: cytosol fraction. Scale bars: mean ± SEM of three independent experiments. ** p < 0.01 compared to vehicle-treated control cells, C) Representative Western blot showing the induction of phosphorylation of eukaryotic initiation factor-2 (eIF-2) in A549 cells treated with GI50 amounts of compound 5. For comparison purposes, thapsigargin (TG), an ER stress-causing drug was used (3 μM, 2 h) as a positive control. The experiment was repeated three times.
Figure 4 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654
Figure 4 Compound 5 causes caspase activation. A) qRT-PCR analysis of caspase 3, 4, 8 and 9 mRNA in compound 5-treated cells (GI50) as compared to vehicle-treated control cells [set as 1 arbitrary unit (a.u.)]. Values were normalized to β-actin. Scale bars: mean ± SEM of three independent experiments performed in triplicates. *p < 0.05, **p < 0.01 compared to vehicle-treated control cells, B) Representative Western blots showing cleavage "activation' of procaspase 3 to the active form p17, procaspase 4 to the active form p20, and procaspase 9 to the active forms p35/p37. C: vehicle-treated control cells; 0.5%: 0.5% DMSO-treated cells; 1%: 1% DMSO-treated cells; 5%: 5% DMSO-treated cells; C.5: Compound 5-treated cells. The experiment was repeated three times.
Figure 2 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654
Figure 2 The MTT (3-(4,5-dimethylthiazol-2-yl)-2,5 diphenyltetrazolium bromide) assay results for compound 5 against MCF10A cells, and white blood cells (WBC) after 24, 48 and 72 h of treatment.
Figure 3 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654
Figure 3 Compound 5 induces apoptosis in A549 lung cancer cells. A) Fluorescence images of A549 lung cancer cells showing fragmented nuclei after DAPI staining. Scale bar: 10 µm, B) Detection of DNA fragmentation by agarose gel electrophoresis. Cells were treated and genomic DNA was extracted and electrophoresed on 1.5% agarose gels. M: DNA molecular weight marker; C: vehicle-treated control cells; 1%: 1% DMSO-treated cells; 5%: 5% DMSO-treated cells; C.5: Compound 5-treated cells. Arrows indicate DNA fragments. Three experiments were performed with similar results.
Figure 3 from: Kokanova-Nedialkova Z, Aluani D, Tzankova V, Nedialkov P (2021) Simultaneous quantification of the major flavonoids from wild spinach by UHPLC-HRMS and their neuroprotective effects in a model of H2O2-induced oxidative stress on SH-SY5Y cells. Pharmacia 68(3): 657-664. https://doi.org/10.3897/pharmacia.68.e71030
Figure 3 Effect of flavonoids and silibinin on the viability of SH-SY5Y cells in a model of H2O2-induced toxicity. Data are presented as means from three independent experiments ± SD (n = 8). ***P < 0.001, vs. untreated control; +++P < 0.001, vs. H2O2 group. (one-way analysis of variance with Dunnet's post hoc test).
Figure 6 from: Abbas AH, Mahmood AAR, Tahtamouni LH, Al-Mazaydeh ZA, Rammaha MS, Alsoubani F, Al-bayati RI (2021) A novel derivative of picolinic acid induces endoplasmic reticulum stress-mediated apoptosis in human non-small cell lung cancer cells: synthesis, docking study, and anticancer activity. Pharmacia 68(3): 679-692. https://doi.org/10.3897/pharmacia.68.e70654
Figure 6 3D View of the target compounds (5, 7A, 6B and 6C) docked against ATP binding site of EGFR kinase.
Fig. 3 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 3. Experimental ECD spectra of compound 9.
Fig. 2 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 2. Key HMBC correlations of compounds 1–11.
Fig. 1 in Verniciflavanol A, a profisetinidin-type-4-arylflavan-3-ol from toxicodendron vernicifluum protects SH-SY5Y cells against H2O2-Induced oxidative stress
Fig. 1. The structures of compounds 1–19.
Fig. 2 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress
Fig. 2. Key HMBC correlations of compounds 1–5.
Fig. 1 in Phenolics from Archidendron clypearia (Jack) I.C.Nielsen protect SH-SY5Y cells against H O -induced oxidative stress
Fig. 1. The structures of compounds 1–18.
Clinical Study of Hypoxia-Stressed Bone Marrow Mononuclear Cell Transplantation to Treat Heart Diseases
ClinicalTrials.gov study NCT01234181. IPD Sharing: Not stated. Countries: 0. Publications: 2.
Autologous Cell Therapy for Stress Urinary Incontinence in Males Following Prostate Surgery
ClinicalTrials.gov study NCT02291432. IPD Sharing: NO. Countries: 1. Publications: 0.
Feasibility of a Stress Reduction Intervention Study in Sickle Cell Disease
ClinicalTrials.gov study NCT02501447. IPD Sharing: Not stated. Countries: 0. Publications: 1.
Autologous Cell Therapy for Female Stress Urinary Incontinence
ClinicalTrials.gov study NCT01008943. IPD Sharing: Not stated. Countries: 1. Publications: 0.
An Investigation of the Safety of 4 Different Doses of Autologous Muscle Derived Cells as Therapy for Stress Urinary Incontinence
ClinicalTrials.gov study NCT00847535. IPD Sharing: Not stated. Countries: 2. Publications: 0.
The Stress-release Effects of Exercise in Obese Are Determined by DS14 Score and T-cell Activation Status
ClinicalTrials.gov study NCT02493413. IPD Sharing: Not stated. Countries: 0. Publications: 22.
Data from: Nitric oxide signals are interlinked with calcium signals in normal pancreatic stellate cells upon oxidative stress and inflammation
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International Brain Laboratory public data
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OpenNeuro
OpenNeuro is a free, open platform for sharing neuroimaging datasets, with public search, dataset pages, and download paths for web, S3, DataLad, and the OpenNeuro CLI.