Search results for "Dative"

showing 10 items of 2381 documents

Oxidative Stress and Vascular Dysfunction in the Retina: Therapeutic Strategies

2020

Many retinal diseases, such as diabetic retinopathy, glaucoma, and age-related macular (AMD) degeneration, are associated with elevated reactive oxygen species (ROS) levels. ROS are important intracellular signaling molecules that regulate numerous physiological actions, including vascular reactivity and neuron function. However, excessive ROS formation has been linked to vascular endothelial dysfunction, neuron degeneration, and inflammation in the retina. ROS can directly modify cellular molecules and impair their function. Moreover, ROS can stimulate the production of inflammatory cytokines, such as tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6) causing inflammation and cel…

0301 basic medicineCell signalingProgrammed cell deathPhysiologyClinical BiochemistryInflammationReviewmedicine.disease_causeBiochemistryProinflammatory cytokine03 medical and health sciences0302 clinical medicinemedicineoxidative stressEndothelial dysfunctionMolecular Biologyreactive oxygen speciesRetinabusiness.industrylcsh:RM1-950Cell Biologymedicine.diseaseCell biology030104 developmental biologymedicine.anatomical_structurelcsh:Therapeutics. Pharmacology030221 ophthalmology & optometryTumor necrosis factor alpharetinal diseasemedicine.symptombusinessvascular endotheliumOxidative stressAntioxidants
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MYC Induces a Hybrid Energetics Program Early in Cell Reprogramming

2018

Summary Cell reprogramming is thought to be associated with a full metabolic switch from an oxidative- to a glycolytic-based metabolism. However, neither the dynamics nor the factors controlling this metabolic switch are fully understood. By using cellular, biochemical, protein array, metabolomic, and respirometry analyses, we found that c-MYC establishes a robust bivalent energetics program early in cell reprogramming. Cells prone to undergo reprogramming exhibit high mitochondrial membrane potential and display a hybrid metabolism. We conclude that MYC proteins orchestrate a rewiring of somatic cell metabolism early in cell reprogramming, whereby somatic cells acquire the phenotypic plast…

0301 basic medicineCell signalingSomatic cellCèl·lulesCellOxidative phosphorylationcell reprogramming cell signaling metabolism mitochondrial dynamicsBiologyHybrid CellsBiochemistryMitochondrial DynamicsArticleOxidative PhosphorylationMitocondrisProto-Oncogene Proteins c-myc03 medical and health sciencesMetabolomicsCDC2 Protein KinaseGeneticsmedicinecell signalingAnimalsHumansGlycolysisPhosphorylationlcsh:QH301-705.5Membrane potentialMembrane Potential Mitochondriallcsh:R5-920cell reprogrammingCell BiologyCellular ReprogrammingCell biologyMitochondriaMice Inbred C57BL030104 developmental biologymedicine.anatomical_structurelcsh:Biology (General)lcsh:Medicine (General)ReprogrammingmetabolismGlycolysisDevelopmental Biology
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The Role of Iron in Friedreich's Ataxia: Insights From Studies in Human Tissues and Cellular and Animal Models.

2019

Friedreich’s ataxia (FRDA) is a rare early-onset degenerative disease that affects both the central and peripheral nervous systems, and other extraneural tissues, mainly the heart and endocrine pancreas. This disorder progresses as a mixed sensory and cerebellar ataxia, primarily disturbing the proprioceptive pathways in the spinal cord, peripheral nerves and nuclei of the cerebellum. FRDA is an inherited disease with an autosomal recessive pattern caused by an insufficient amount of the nuclear-encoded mitochondrial protein frataxin, which is an essential and highly evolutionary conserved protein whose deficit results in iron metabolism dysregulation and mitochondrial dysfunction. The firs…

0301 basic medicineCerebellumAtaxiaFriedreich’s ataxiaReviewMitochondrionmedicine.disease_causelcsh:RC321-57103 medical and health sciencesiron0302 clinical medicineDegenerative diseasemedicineoxidative stresslcsh:Neurosciences. Biological psychiatry. Neuropsychiatrychemistry.chemical_classificationReactive oxygen speciesfrataxinbiologyCerebellar ataxialipid deregulationGeneral Neurosciencemedicine.diseaseanimal modelsCell biology030104 developmental biologymedicine.anatomical_structurechemistryFrataxinbiology.proteiniron chelatorsmedicine.symptom030217 neurology & neurosurgeryOxidative stressNeuroscienceFrontiers in neuroscience
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A Drosophila model of GDAP1 function reveals the involvement of insulin signalling in the mitochondria-dependent neuromuscular degeneration

2017

[EN] Charcot-Marie-Tooth disease is a rare peripheral neuropathy for which there is no specific treatment. Some forms of Charcot-Marie-Tooth are due to mutations in the GDAP1 gene. A striking feature of mutations in GDAP1 is that they have a variable clinical manifestation, according to disease onset and progression, histology and mode of inheritance. Studies in cellular and animal models have revealed a role of GDAP1 in mitochondrial morphology and distribution, calcium homeostasis and oxidative stress. To get a better understanding of the disease mechanism we have generated models of over-expression and RNA interference of the Drosophila Gdapl gene. In order to get an overview about the c…

0301 basic medicineCharcot-Marie-Toothmedicine.medical_treatmentNerve Tissue ProteinsGDAP1MitochondrionBiologymedicine.disease_cause03 medical and health sciencesCharcot-Marie-Tooth DiseaseRNA interferenceGene expressionBIOQUIMICA Y BIOLOGIA MOLECULARmedicineAnimalsDrosophila ProteinsHumansInsulinMolecular BiologyGeneticsMechanism (biology)InsulinNeurodegenerationLipid Metabolismmedicine.diseaseUp-RegulationMitochondriaCell biology030104 developmental biologyMetabolomeCarbohydrate MetabolismMolecular MedicineDrosophilaRNA InterferenceOxidative stressFunction (biology)Signal TransductionBiochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
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CD4+ T-cell differentiation and function: Unifying glycolysis, fatty acid oxidation, polyamines NAD mitochondria

2021

The progression through different steps of T-cell development, activation, and effector function is tightly bound to specific cellular metabolic processes. Previous studies established that T-effector cells have a metabolic bias toward aerobic glycolysis, whereas naive and regulatory T cells mainly rely on oxidative phosphorylation. More recently, the field of immunometabolism has drifted away from the notion that mitochondrial metabolism holds little importance in T-cell activation and function. Of note, T cells possess metabolic promiscuity, which allows them to adapt their nutritional requirements according to the tissue environment. Altogether, the integration of these metabolic pathway…

0301 basic medicineChemistryCatabolismImmunologyOxidative phosphorylationMitochondrionCell biologyCitric acid cycle03 medical and health sciencesMetabolic pathway030104 developmental biology0302 clinical medicineAnaerobic glycolysis030220 oncology & carcinogenesisImmunology and AllergyGlycolysisBeta oxidationJournal of Allergy and Clinical Immunology
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Bevacizumab diminishes inflammation in an acute endotoxin-induced uveitis model

2017

Este artículo se encuentra disponible en la página web de la revista en la siguiente URL: https://www.frontiersin.org/articles/10.3389/fphar.2018.00649/full Introduction: Uveitis is an eye disease characterized by inflammation of the uvea and an early and exhaustive diagnosis is essential for its treatment. The aim of our study is to assess the potential toxicity and anti-inflammatory efficacy of Bevacizumab in an experimental uveitis model by subcutaneously injecting lipopolysaccharide into Lewis rats and to clarify its mechanism. Material and Methods: Blood–aqueous barrier integrity was assessed 24 h after endotoxin-induced uveitis (EIU) by analyzing two parameters: cell count and protein…

0301 basic medicineChemokineLipopolysaccharidegenetic structuresmedicine.medical_treatmentÚvea - Efectos de los medicamentos.chemokinesPharmacologymedicine.disease_causeendotoxin-induced uveitischemistry.chemical_compound0302 clinical medicineMedicineoxidative stressPharmacology (medical)Bevacizumab - Efectos fisiológicos.Bevacizumab - Efectos secundarios.Uvea - Effect of drugs on.Original ResearchEstrés oxidativo.biologyOxidative stress.medicine.anatomical_structureCytokineToxicityOjos - Enfermedades - Tratamiento.medicine.symptomUveitisPharmacology.InflammationFarmacología.bevacizumabBevacizumab - Physiological effect.Bevacizumab - Side effects.03 medical and health sciencesUveitis - Treatment.Eyes - Diseases - Treatment.Pharmacologybusiness.industrylcsh:RM1-950Uveítis - Tratamiento.Uveamedicine.diseaseeye diseasescytokines030104 developmental biologylcsh:Therapeutics. Pharmacologychemistryinflammation030221 ophthalmology & optometrybiology.proteinsense organsbusinessOxidative stress
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Dual proteotoxic stress accelerates liver injury via activation of p62‐Nrf2

2021

Protein accumulation is the hallmark of various neuronal, muscular, and other human disorders. It is also often seen in the liver as a major protein-secretory organ. For example, aggregation of mutated alpha1-antitrypsin (AAT), referred to as PiZ, is a characteristic feature of AAT deficiency, whereas retention of hepatitis B surface protein (HBs) is found in chronic hepatitis B (CHB) infection. We investigated the interaction of both proteotoxic stresses in humans and mice. Animals overexpressing both PiZ and HBs (HBs-PiZ mice) had greater liver injury, steatosis, and fibrosis. Later they exhibited higher hepatocellular carcinoma load and a more aggressive tumor subtype. Although PiZ and H…

0301 basic medicineCirrhosisNF-E2-Related Factor 2medicine.disease_causePathology and Forensic MedicineMice03 medical and health sciences0302 clinical medicineSDG 3 - Good Health and Well-beingStress PhysiologicalFibrosisSequestosome-1 ProteinmedicineAnimalsHumansLiver injuryHepatitis B Surface Antigensbusiness.industryLiver DiseasesAutophagyHepatitis Bmedicine.diseasedigestive system diseasesaggregate Hepatitis B Surface Antigens Humans Liver Diseases Mice NF-E2-Related Factor 2 Sequestosome-1 Protein Stress Physiological alpha 1-Antitrypsin cirrhosis inclusionlipophagy oxidative stress SERPINA1 Animals030104 developmental biologyalpha 1-Antitrypsin030220 oncology & carcinogenesisHepatocellular carcinomaCancer researchSteatosisbusinessOxidative stressThe Journal of Pathology
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Impact of high-pressure processing on the stability and bioaccessibility of bioactive compounds in Clementine mandarin juice and its cytoprotective e…

2020

Mandarin juice is a rich source of antioxidant bioactive compounds. While the content and profile of bioactives are known, the impact of high-pressure processing (HPP) on their stability and bioaccessibility (BA) is unknown, but may allow obtaining safe, nutritious, and fresh-tasting juices with highly extractable bioactive compounds. The stability and BA of bioactive antioxidant compounds in untreated and HPP-treated (400 MPa/40 °C/1 min) Clementine mandarin juices, and the cytoprotective effect of its bioaccessible fractions (BF) obtained after simulated gastrointestinal digestion against H2O2-induced oxidative stress in differentiated Caco-2 cells were investigated. The BF of HPP-treated…

0301 basic medicineCitrusAntioxidantFood Handlingmedicine.medical_treatmentPhytochemicalsBiological AvailabilityPascalization03 medical and health sciences0404 agricultural biotechnologyCryoprotective AgentsAntioxidant activitymedicineHumansBeta-cryptoxanthinFood scienceOrange juiceCarotenoidchemistry.chemical_classificationOrange juicePulsed electric-fields030109 nutrition & dieteticsVitamin CVitamin-c04 agricultural and veterinary sciencesGeneral MedicineAscorbic acid040401 food scienceCytoprotectionIn-vitro bioaccessibilityFlavonoid compositionFruit and Vegetable JuiceschemistryPolyphenolOxidative stressCitrus juiceAscorbic acidCaco-2 CellsFood ScienceFoodfunction
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The potential of aldehyde dehydrogenase 2 as a therapeutic target in cardiovascular disease.

2018

Mitochondrial aldehyde dehydrogenase (ALDH-2) plays a major role in the ethanol detoxification pathway by removing acetaldehyde. Therefore, ALDH-2 inhibitors such as disulfiram represent the first therapeutic targeting of ALDH-2 for alcoholism therapy. Areas covered: Recently, ALDH-2 was identified as an essential bioactivating enzyme of the anti-ischemic organic nitrate nitroglycerin, bringing ALDH-2 again into the focus of clinical interest. Mechanistic studies on the nitroglycerin bioactivation process revealed that during bioconversion of nitroglycerin and in the presence of reactive oxygen and nitrogen species the active site thiols of ALDH-2 are oxidized and the enzyme activity is los…

0301 basic medicineClinical BiochemistryAldehyde dehydrogenasemedicine.disease_causeAntioxidants03 medical and health scienceschemistry.chemical_compoundDetoxificationDrug DiscoverymedicineAnimalsHumansMolecular Targeted TherapyPharmacologyEthanolbiologyAldehyde Dehydrogenase MitochondrialMitochondrial Aldehyde DehydrogenaseAcetaldehydeCardiovascular AgentsDisease Models AnimalOxidative Stress030104 developmental biologyBiochemistrychemistryCardiovascular DiseasesDrug DesignCardiovascular agentDisulfirambiology.proteinMolecular MedicineOxidative stressmedicine.drugExpert opinion on therapeutic targets
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Enhanced autophagic-lysosomal activity and increased BAG3-mediated selective macroautophagy as adaptive response of neuronal cells to chronic oxidati…

2019

Oxidative stress and a disturbed cellular protein homeostasis (proteostasis) belong to the most important hallmarks of aging and of neurodegenerative disorders. The proteasomal and autophagic-lysosomal degradation pathways are key measures to maintain proteostasis. Here, we report that hippocampal cells selected for full adaptation and resistance to oxidative stress induced by hydrogen peroxide (oxidative stress-resistant cells, OxSR cells) showed a massive increase in the expression of components of the cellular autophagic-lysosomal network and a significantly higher overall autophagic activity. A comparative expression analysis revealed that distinct key regulators of autophagy are upregu…

0301 basic medicineClinical BiochemistryLFQ Label-free quantificationLETM Leucine zipper and EF-hand containing transmembrane proteinmedicine.disease_causeBiochemistryCHX Cycloheximide0302 clinical medicineBNIP3 Bcl-2 interacting protein 3RAPA RapamycinPIK3C3 Class III PI3‐kinasePhosphorylationlcsh:QH301-705.5Neuronslcsh:R5-920PolyUB PolyubiquitinChemistryBAG3OPA1 Optic atrophy 1TOR Serine-Threonine KinasesWIPI1 WD repeat domain phosphoinositide-interacting protein 1ATG Autophagy relatedTFEB Transcription factor EBCell biologyMitochondriasiRNA Small interfering RNADLP1 Dynamin-like protein 1LAMP1 Lysosomal‐associated membrane protein 1PURO Puromycinlcsh:Medicine (General)Protein homeostasisResearch PaperBafA1 Bafilomycin A1LAMP2 Lysosomal‐associated membrane protein 2Proteasome Endopeptidase ComplexRAB18 Member RAS oncogeneTUB TubulinLC3 Light chain 3 proteinOxidative phosphorylationBAG3CTSD Cathepsin DModels BiologicalCell Line03 medical and health sciencesDownregulation and upregulationMacroautophagymedicineAutophagyHumansAdaptationBAG1 Bcl-2-associated athanogene 1BECN1 Beclin1PI3K/AKT/mTOR pathwayAdaptor Proteins Signal TransducingTEM Transmission electron microscopyHsp70 Heat shock protein 70Organic ChemistryAutophagyAutophagosomesmTOR Mammalian target of rapamycinHsp70Oxidative Stress030104 developmental biologyProteostasislcsh:Biology (General)CV CanavanineBAG3 Bcl-2-associated athanogene 3MTT (3-(45-Dimethylthiazol-2-yl)-25-Diphenyltetrazolium Bromide)Apoptosis Regulatory ProteinsLysosomes030217 neurology & neurosurgeryOxidative stressRedox Biology
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