Search results for "Stress."

showing 10 items of 5934 documents

The fear-defense system, emotions, and oxidative stress

2020

Psychosocial stress has a profound impact on well-being and health. The response to stress is associated mainly with the amygdala, a crucial structure of the fear-defense system, essential for social cognition and emotion regulation. Recent neuroimaging-studies demonstrated how an increased metabolic activity of the amygdala enhances inflammation, and leads to cardiometabolic disease. The development of therapeutic strategies depends on our understanding of both which factors activate the fear-defense system and the subsequent molecular mechanisms that translate emotional stress into cell damage. Fear of emotions as an aftermath of attachment trauma is the most important trigger of the mala…

0301 basic medicineFear-defense systemEmotionsClinical BiochemistryInflammationAnxietymedicine.disease_causeBiochemistryAmygdalaProinflammatory cytokine03 medical and health sciences0302 clinical medicineSocial cognitionmedicineHumanslcsh:QH301-705.5Cell damageInflammationlcsh:R5-920business.industryOrganic ChemistryFearAmygdalamedicine.diseaseGraphical ReviewOxidative Stress030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)Anxietymedicine.symptomlcsh:Medicine (General)businessNeuroscience030217 neurology & neurosurgeryGlucocorticoidOxidative stressmedicine.drugRedox Biology
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Erwinia amylovora psychrotrophic adaptations: evidence of pathogenic potential and survival at temperate and low environmental temperatures

2017

The fire blight pathogenErwinia amylovoracan be considered a psychrotrophic bacterial species since it can grow at temperatures ranging from 4 °C to 37 °C, with an optimum of 28 °C. In many plant pathogens the expression of virulence determinants is restricted to a certain range of temperatures. In the case ofE. amylovora,temperatures above 18 °C are required for blossom blight epidemics under field conditions. Moreover, this bacterium is able to infect a variety of host tissues/organs apart from flowers, but it is still unknown how environmental temperatures, especially those below 18 °C, affect the pathogen ability to cause fire blight disease symptoms in such tissues/organs. There is als…

0301 basic medicineFire blight030106 microbiologylcsh:MedicineVirulenceSiderophoresBiologyErwiniaMicrobiologyGeneral Biochemistry Genetics and Molecular BiologyViable but nonculturableMicrobiologyVBNC03 medical and health sciencesBlightAgricultural SciencePathogenEcologyVirulenceGeneral Neurosciencelcsh:RBiofilmMotilityGeneral Medicinebiology.organism_classificationOxidative stressStarvationBiofilmsFire blightEPSGeneral Agricultural and Biological SciencesBacteriaPeerJ
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Visualizing the spatiotemporal map of Rac activation in bovine aortic endothelial cells under laminar and disturbed flows.

2017

Disturbed flow can eliminate the alignment of endothelial cells in the direction of laminar flow, and significantly impacts on atherosclerosis in collateral arteries near the bifurcation and high curvature regions. While shear stress induced Rac polarity has been shown to play crucial roles in cell polarity and migration, little is known about the spatiotemporal map of Rac under disturbed flow, and the mechanism of flow-induced cell polarity still needs to be elucidated. In this paper, disturbed flow or laminar flow with 15 dyn/cm2 of average shear stress was applied on bovine aortic endothelial cells (BAECs) for 30 minutes. A genetically-encoded PAK-PBD-GFP reporter was transfected into BA…

0301 basic medicineFluorescence-lifetime imaging microscopyCell Membraneslcsh:MedicineMicrotubulesCell membraneLaminar Flow0302 clinical medicineCell polarityFluorescence microscopeMembrane fluidityCytoskeletonlcsh:ScienceShear StressesCytoskeletonAortaMultidisciplinaryChemistryPhysicsClassical MechanicsCell Polarityrac GTP-Binding Proteinsmedicine.anatomical_structurePhysical SciencesMechanical StressCellular Structures and OrganellesResearch ArticleCell PhysiologyImaging TechniquesMembrane FluidityFluid MechanicsResearch and Analysis MethodsContinuum Mechanics03 medical and health sciencesFluorescence ImagingShear stressmedicineAnimalsFluid Flowlcsh:RBiology and Life SciencesFluid DynamicsLaminar flowCell Biology030104 developmental biologyBiophysicsCattlelcsh:QEndothelium Vascular030217 neurology & neurosurgeryPLoS ONE
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Transcriptional Changes after Enniatins A, A1, B and B1 Ingestion in Rat Stomach, Liver, Kidney and Lower Intestine

2021

Enniatins (ENs) are depsipeptide mycotoxins produced by Fusarium fungi. They are known for their capacity to modulate cell membrane permeability and disruption of ionic gradients, affecting cell homeostasis and initiating oxidative stress mechanisms. The effect of the acute toxicity of ENs A, A1, B and B1 at two different concentrations after 8 h of exposure was analysed in Wistar rats by a transcriptional approach. The following key mitochondrial and nuclear codified genes related to the electron transport chain were considered for gene expression analysis in stomach, liver, kidney and lower intestine by quantitative Real-Time PCR: mitochondrially encoded NADH dehydrogenase 1 (MT-ND1), mit…

0301 basic medicineGPX1Health (social science)oxidative phosphorylationPlant ScienceOxidative phosphorylationTP1-1185medicine.disease_causeOccludinHealth Professions (miscellaneous)Microbiologyquantitative Real-Time PCR (qPCR)Article03 medical and health sciences0404 agricultural biotechnologyenniatinsGene expressionmedicineCytochrome c oxidasebiologyChemistryenniatins; oxidative phosphorylation; in vivo; quantitative Real-Time PCR (qPCR)Succinate dehydrogenaseChemical technology04 agricultural and veterinary sciencesSalut pública040401 food scienceMolecular biologyHeme oxygenasein vivo030104 developmental biologybiology.proteinOxidative stressFood ScienceFoods
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Redox signaling in the gastrointestinal tract.

2017

Redox signaling regulates physiological self-renewal, proliferation, migration and differentiation in gastrointestinal epithelium by modulating Wnt/β-catenin and Notch signaling pathways mainly through NADPH oxidases (NOXs). In the intestine, intracellular and extracellular thiol redox status modulates the proliferative potential of epithelial cells. Furthermore, commensal bacteria contribute to intestine epithelial homeostasis through NOX1- and dual oxidase 2-derived reactive oxygen species (ROS). The loss of redox homeostasis is involved in the pathogenesis and development of a wide diversity of gastrointestinal disorders, such as Barrett's esophagus, esophageal adenocarcinoma, peptic ulc…

0301 basic medicineGastrointestinal DiseasesNotch signaling pathwaymedicine.disease_causeBiochemistryGastrointestinal epitheliumSuperoxide dismutase03 medical and health scienceschemistry.chemical_compoundPhysiology (medical)medicineHumansSulfhydryl CompoundsIntestinal MucosaWnt Signaling PathwayCell Proliferationchemistry.chemical_classificationReactive oxygen speciesbiologySuperoxideWnt signaling pathwayNADPH OxidasesDual oxidase 2digestive system diseasesGastrointestinal TractIntestinesOxidative Stress030104 developmental biologychemistryImmunologybiology.proteinCancer researchReactive Oxygen SpeciesOxidation-ReductionOxidative stressFree radical biologymedicine
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Oxidative stress-mediated alterations in histone post-translational modifications

2021

Abstract Epigenetic regulation of gene expression provides a finely tuned response capacity for cells when undergoing environmental changes. However, in the context of human physiology or disease, any cellular imbalance that modulates homeostasis has the potential to trigger molecular changes that result either in physiological adaptation to a new situation or pathological conditions. These effects are partly due to alterations in the functionality of epigenetic regulators, which cause long-term and often heritable changes in cell lineages. As such, free radicals resulting from unbalanced/extended oxidative stress have been proved to act as modulators of epigenetic agents, resulting in alte…

0301 basic medicineGene ExpressionContext (language use)Biologymedicine.disease_causeBiochemistryEpigenesis GeneticHistones03 medical and health sciences0302 clinical medicinePhysiology (medical)Gene expressionmedicineHumansHistone codeEpigeneticsRegulation of gene expressionDNA MethylationChromatinCell biologyOxidative Stress030104 developmental biologyHistonebiology.proteinProtein Processing Post-Translational030217 neurology & neurosurgeryOxidative stressFree Radical Biology and Medicine
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NOX2ko Mice Show Largely Increased Expression of a Mutated NOX2 mRNA Encoding an Inactive NOX2 Protein

2020

Background: The superoxide-generating enzyme nicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2 or gp91phox, the phagocytic isoform) was reported as a major source of oxidative stress in various human diseases. Genetic deletion is widely used to study the impact of NOX2-derived reactive oxygen species (ROS) on disease development and progression in various animal models. Here, we investigate why NOX2 knockout mice show no NOX2 activity but express NOX2 mRNA and protein. Methods and Results: Oxidative burst (NOX2-dependent formation of ROS) was measured by L-012-based chemiluminescence and was largely absent in whole blood of NOX2 knockout mice. Protein expression was still de…

0301 basic medicineGene isoformPhysiologyClinical Biochemistrynext generation sequencing (NGS)030204 cardiovascular system & hematologymedicine.disease_causeBiochemistryArticlenicotinamide adenine dinucleotide phosphate (NADPH) oxidase (NOX2) knockout mice03 medical and health scienceschemistry.chemical_compound0302 clinical medicineWestern blotmedicineMolecular BiologyGeneMessenger RNAmedicine.diagnostic_testurogenital systemCell BiologyMolecular biologyRespiratory burst030104 developmental biologychemistryKnockout mousecardiovascular systemoxidative stress related diseasetruncated and inactive mutanthormones hormone substitutes and hormone antagonistsOxidative stressNicotinamide adenine dinucleotide phosphatecirculatory and respiratory physiologyAntioxidants
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RINT1 Loss Impairs Retinogenesis Through TRP53-Mediated Apoptosis

2020

Genomic instability in the central nervous system (CNS) is associated with defective neurodevelopment and neurodegeneration. Congenital human syndromes that affect the CNS development originate from mutations in genes of the DNA damage response (DDR) pathways. RINT1 (Rad50-interacting protein 1) is a partner of RAD50, that participates in the cellular responses to DNA double-strand breaks (DSB). Recently, we showed that Rint1 regulates cell survival in the developing brain and its loss led to premature lethality associated with genomic stability. To bypass the lethality of Rint1 inactivation in the embryonic brain and better understand the roles of RINT1 in CNS development, we conditionally…

0301 basic medicineGenome instabilityDNA damagereplicative stressBiologyDNA damage responseRetinal ganglionganglion cellsCell and Developmental Biology03 medical and health sciences0302 clinical medicinemedicineoptic nerve hypoplasiaProgenitor celllcsh:QH301-705.5Original ResearchNeurogenesisNeurodegenerationneurodegenerationCell BiologyCell cyclemedicine.diseaseNeural stem cellCell biologyneurogenesis030104 developmental biologylcsh:Biology (General)030220 oncology & carcinogenesisvisual system developmentDevelopmental BiologyFrontiers in Cell and Developmental Biology
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A dual role of caspase-8 in triggering and sensing proliferation-associated DNA damage, a key determinant of liver cancer development.

2017

Summary Concomitant hepatocyte apoptosis and regeneration is a hallmark of chronic liver diseases (CLDs) predisposing to hepatocellular carcinoma (HCC). Here, we mechanistically link caspase-8-dependent apoptosis to HCC development via proliferation- and replication-associated DNA damage. Proliferation-associated replication stress, DNA damage, and genetic instability are detectable in CLDs before any neoplastic changes occur. Accumulated levels of hepatocyte apoptosis determine and predict subsequent hepatocarcinogenesis. Proliferation-associated DNA damage is sensed by a complex comprising caspase-8, FADD, c-FLIP, and a kinase-dependent function of RIPK1. This platform requires a non-apop…

0301 basic medicineGenome instabilityMaleliver; Hepatocellular carcinoma; DNA damage response; replication stress; apoptosisCancer ResearchDNA RepairCarcinogenesisFas-Associated Death Domain ProteinApoptosisurologic and male genital diseasesDNA damage responseDna Damage Response ; Apoptosis ; Hepatocellular Carcinoma ; Liver ; Replication StressHistonesMice0302 clinical medicineRisk FactorsFADDPhosphorylationCellular SenescenceCaspase 8biologyLiver Neoplasmshepatocellular carcinomaLiver regeneration3. Good healthHistoneOncologyReceptors Tumor Necrosis Factor Type I030220 oncology & carcinogenesisReceptor-Interacting Protein Serine-Threonine KinasesFemalebiological phenomena cell phenomena and immunityCell agingCarcinoma HepatocellularDNA damageDNA repairreplication stressCaspase 8liverArticleGenomic Instability03 medical and health sciencesAnimalsHepatectomyHumansCrosses GeneticCell ProliferationJNK Mitogen-Activated Protein KinasesCell BiologyLiver Regeneration030104 developmental biologyImmunologyChronic Diseasebiology.proteinCancer researchHepatocytesMyeloid Cell Leukemia Sequence 1 ProteinDNA Damage
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FANCD2 modulates the mitochondrial stress response to prevent common fragile site instability

2021

Common fragile sites (CFSs) are genomic regions frequently involved in cancer-associated rearrangements. Most CFSs lie within large genes, and their instability involves transcription- and replication-dependent mechanisms. Here, we uncover a role for the mitochondrial stress response pathway in the regulation of CFS stability in human cells. We show that FANCD2, a master regulator of CFS stability, dampens the activation of the mitochondrial stress response and prevents mitochondrial dysfunction. Genetic or pharmacological activation of mitochondrial stress signaling induces CFS gene expression and concomitant relocalization to CFSs of FANCD2. FANCD2 attenuates CFS gene transcription and pr…

0301 basic medicineGenome instabilitymusculoskeletal diseasesTranscription GeneticQH301-705.5RegulatorMedicine (miscellaneous)MitochondrionBiology[SDV.BBM.BM] Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyGeneral Biochemistry Genetics and Molecular BiologyOxidative PhosphorylationArticle03 medical and health sciences0302 clinical medicineTranscription (biology)Stress Physiologicalhemic and lymphatic diseasesGene expressionFANCD2HumansBiology (General)GeneUbiquitinsChromosomal fragile siteChromosome Fragile SitesChromosome FragilityFanconi Anemia Complementation Group D2 ProteinDNA damage and repair[SDV.BBM.BM]Life Sciences [q-bio]/Biochemistry Molecular Biology/Molecular biologyHCT116 CellsCell biologyMitochondriaSettore BIO/18 - Genetica030104 developmental biologyGene Expression Regulation030220 oncology & carcinogenesisUnfolded Protein ResponseGeneral Agricultural and Biological SciencesDNA Damage
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