Search results for "Endothelial Cells"

showing 10 items of 441 documents

Human neutrophil elastase induces endothelial cell apoptosis by activating the PERK‐CHOP branch of the unfolded protein response

2017

Human neutrophil elastase impacts on atherosclerotic plaque stability by inducing apoptosis in endothelial cells. Our aim was to investigate the proapoptotic mechanism of elastase on endothelial cells and to evaluate the presence of elastase in human plaque material. Human endothelial cells were treated with purified human neutrophil elastase. Apoptosis was assayed by capsase-3/7 activation, TUNEL, and sub-G1 assay. Activation of unfolded protein response (UPR) effector molecules binding Ig protein, soluble X-binding protein-1, protein kinase RNA-like ER kinase (PERK), and C/EBP-homologous protein (CHOP) was analyzed by RT-PCR, immunocytochemistry, and Western blot. Genetic silencing of CHO…

0301 basic medicineSmall interfering RNACell SurvivalApoptosisCHOPBiochemistryGene Expression Regulation EnzymologicCell LineeIF-2 Kinase03 medical and health sciencesGeneticsHumansReceptor PAR-2Receptor PAR-1Protein kinase AMolecular BiologyCaspase 7Caspase 3KinaseChemistryElastaseEndothelial CellsAtherosclerosisMolecular biologyEndothelial stem cellCarotid Arteries030104 developmental biologyApoptosisUnfolded Protein ResponseUnfolded protein responseLeukocyte ElastaseTranscription Factor CHOPBiotechnologyThe FASEB Journal
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Comparative study of the production of soluble factors in human placenta-derived mesenchymal stromal/stem cells grown in adherent conditions or as ag…

2019

Abstract Different approaches have been studied in both preclinical and clinical settings to develop cell-based therapies and/or engineered cell-based therapies to better integrate grafts with the host. In these techniques, much attention is addressed to the use of adult stem cells such as mesenchymal stem cells (MSCs), but identifying and obtaining sufficient numbers of therapeutic cells, and the right route of administration, is often a challenge. In this study, we tested the feasibility of encapsulating human amnion-derived MSCs (hAMSCs) in a semipermeable and biocompatible fiber as a new approach for regenerative medicine. Our data showed that hAMSCs aggregated in the device constitutes…

0301 basic medicineStromal cellAngiogenesisCell SurvivalPlacentaCellBiophysicsCell Culture TechniquesBiocompatible MaterialsBiologyParacrine effectsBiochemistryRegenerative medicineImmunomodulation03 medical and health sciences0302 clinical medicineImmune systemCell MovementPregnancymedicineCell AdhesionHuman Umbilical Vein Endothelial CellsHumansImmunologic FactorsAmnionMolecular BiologyCell AggregationSettore MED/04 - Patologia GeneraleCatheter-like devicePlacenta-derived stromal/stem cellsSettore BIO/16 - Anatomia UmanaMesenchymal stem cellMesenchymal Stem CellsCell BiologyCells Immobilized030104 developmental biologymedicine.anatomical_structure030220 oncology & carcinogenesisRegenerative medicineCancer researchAngiogenesis Inducing AgentsFemaleAngiogenesisStem cellAdult stem cell
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Identification of neuronal and angiogenic growth factors in an in vitro blood-brain barrier model system: Relevance in barrier integrity and tight ju…

2016

We previously demonstrated that the co-cultivation of endothelial cells with neural cells resulted in an improved integrity of the in vitro blood-brain barrier (BBB), and that this model could be useful to evaluate the transport properties of potential central nervous system disease drugs through the microvascular brain endothelial. In this study we have used real-time PCR, fluorescent microscopy, protein arrays and enzyme-linked immunosorbent assays to determine which neural- and endothelial cell-derived factors are produced in the co-culture and improve the integrity of the BBB. In addition, a further improvement of the BBB integrity was achieved by adjusting serum concentrations and grow…

0301 basic medicineSus scrofaCell Culture TechniquesCell CommunicationBiologyMatrix metalloproteinaseBlood–brain barrierBiochemistryTight JunctionsCapillary Permeability03 medical and health sciences0302 clinical medicinePEDFIn vivoNeurotrophic factorsCell Line TumormedicineElectric ImpedanceAnimalsHumansNerve Growth FactorsAngiogenic ProteinsNeuronsTight Junction ProteinsTight junctionEndothelial CellsCell BiologyCoculture TechniquesCell biologyVascular endothelial growth factor B030104 developmental biologymedicine.anatomical_structurePhenotypeBlood-Brain BarrierImmunologyNeurovascular CouplingEndostatinCardiology and Cardiovascular Medicine030217 neurology & neurosurgerySignal TransductionMicrovascular research
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Oxidative stress in retinal pigment epithelium cells increases exosome secretion and promotes angiogenesis in endothelial cells.

2015

10 páginas, 5 figuras

0301 basic medicineVascular Endothelial Growth Factor AAngiogenesisretinal pigment epitheliumNeovascularization PhysiologicexosomesBiologyExosomesExosomeCell Line03 medical and health sciencesangiogenesismedicineHuman Umbilical Vein Endothelial CellsHumansRNA MessengerRetinal pigment epitheliumVEGF receptorsTube formationRetinal pigment epitheliumEthanolCell BiologyOriginal ArticlesMicrovesicleseye diseasesCell biologyEndothelial stem cellVascular endothelial growth factor AOxidative Stress030104 developmental biologymedicine.anatomical_structureReceptors Vascular Endothelial Growth FactorOxidative stressCell cultureMolecular MedicineOriginal ArticleAngiogenesissense organsJournal of cellular and molecular medicine
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Impact of polymer-modified gold nanoparticles on brain endothelial cells: exclusion of endoplasmic reticulum stress as a potential risk factor

2016

A library of polymer-coated gold nanoparticles (AuNPs) differing in size and surface modifications was examined for uptake and induction of cellular stress responses in the endoplasmic reticulum (ER stress) in human brain endothelial cells (hCMEC/D3). ER stress is known to affect the physiology of endothelial cells (ECs) and may lead to inflammation or apoptosis. Thus, even if applied at non-cytotoxic concentrations ER stress caused by nanoparticles should be prevented to reduce the risk of vascular diseases and negative effects on the integrity of barriers (e.g. blood-brain barrier). We exposed hCMEC/D3 to twelve different AuNPs (three sizes: 18, 35, and 65 nm, each with four surface-modif…

0301 basic medicineXBP1BiPCell SurvivalPolymersBiomedical EngineeringMetal NanoparticlesApoptosis02 engineering and technologyBiologyEndoplasmic ReticulumToxicologyArticleCell LineProinflammatory cytokine03 medical and health sciencescell stressDownregulation and upregulationRisk FactorsHeat shock proteinAnimalsHumansHSP70 Heat-Shock ProteinsParticle SizeHeat-Shock ProteinsATF6Endoplasmic reticulumInterleukin-8ATF4Endothelial CellsMembrane Proteinsunfolded protein responseEndoplasmic Reticulum Stress021001 nanoscience & nanotechnologyQPActivating Transcription Factor 4Cell biology030104 developmental biologyBlood-Brain Barriertight junction proteinsImmunologyUnfolded protein responseGold0210 nano-technologyTranscription Factor CHOPNanotoxicology
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Junctional adhesion molecules JAM-B and JAM-C promote autoimmune-mediated liver fibrosis in mice

2018

Fibrosis remains a serious health concern in patients with chronic liver disease. We recently reported that chemically induced chronic murine liver injury triggers increased expression of junctional adhesion molecules (JAMs) JAM-B and JAM-C by endothelial cells and de novo synthesis of JAM-C by hepatic stellate cells (HSCs). Here, we demonstrate that biopsies of patients suffering from primary biliary cholangitis (PBC), primary sclerosing cholangitis (PSC) or autoimmune hepatitis (AIH) display elevated levels of JAM-C on portal fibroblasts (PFs), HSCs, endothelial cells and cholangiocytes, whereas smooth muscle cells expressed JAM-C constitutively. Therefore, localization and function of JA…

0301 basic medicine[SDV]Life Sciences [q-bio]Cholangitis SclerosingMyocytes Smooth MuscleeducationImmunologyImmunoglobulinsAutoimmune hepatitisVascular RemodelingChronic liver diseaseMural cellPrimary sclerosing cholangitisFatty Acids MonounsaturatedMice03 medical and health sciencesFibrosisCell AdhesionmedicineAnimalsHumansImmunology and AllergyMyofibroblastsCells CulturedInflammationMice KnockoutFibrous capsule of GlissonLiver Cirrhosis Biliarybusiness.industryfungiEndothelial Cellsmedicine.diseaseFibrosishumanities3. Good healthMice Inbred C57BLDisease Models AnimalHepatitis Autoimmune030104 developmental biologyLiverVasoconstrictioncardiovascular systemCancer researchHepatic stellate cellFemaleHepatic fibrosisbusinessCell Adhesion MoleculesJournal of Autoimmunity
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Proteolytic Enzymes Clustered in Specialized Plasma-Membrane Domains Drive Endothelial Cells’ Migration

2016

In vitro cultured endothelial cells forming a continuous monolayer establish stable cell-cell contacts and acquire a "resting" phenotype; on the other hand, when growing in sparse conditions these cells acquire a migratory phenotype and invade the empty area of the culture. Culturing cells in different conditions, we compared expression and clustering of proteolytic enzymes in cells having migratory versus stationary behavior. In order to observe resting and migrating cells in the same microscopic field, a continuous cell monolayer was wounded. Increased expression of proteolytic enzymes was evident in cell membranes of migrating cells especially at sprouting sites and in shed membrane vesi…

0301 basic medicinekalininsepraseCell Membranesbeta1 integrinCelllcsh:MedicineurokinaseBiochemistryEpitheliumCell membrane0302 clinical medicineAnimal CellsMedicine and Health Sciencesdipeptidyl peptidase IVlcsh:ScienceMultidisciplinarybiologyVesicleProteolytic enzymesCell migrationProteasesEnzymesCell biologyLaboratory EquipmentCell Motilitymedicine.anatomical_structureBiochemistry030220 oncology & carcinogenesisEngineering and TechnologyBiological Culturesmatrix metalloproteinase 14Cellular Structures and OrganellesCellular TypesAnatomyResearch ArticleEquipmentCell MigrationResearch and Analysis MethodsGelatin MediaCell Linegelatinase B03 medical and health sciencescollagen type 4fibronectinmedicineHumansVesiclescollagen type 1gelatinase Alcsh:RCell MembraneBiology and Life SciencesEndothelial CellsProteinsMembrane ProteinsEpithelial CellsCell BiologyCulture MediaFibronectinBiological Tissue030104 developmental biologyMembrane proteinCell cultureProteolysisMicroscopy Electron ScanningEnzymologybiology.proteinlcsh:QCollagensDevelopmental BiologyPLOS ONE
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Mitochondrial targeting as a novel therapy for stroke

2018

Stroke is a main cause of mortality and morbidity worldwide. Despite the increasing development of innovative treatments for stroke, most are unsuccessful in clinical trials. In recent years, an encouraging strategy for stroke therapy has been identified in stem cells transplantation. In particular, grafting cells and their secretion products are leading with functional recovery in stroke patients by promoting the growth and function of the neurovascular unit – a communication framework between neurons, their supply microvessels along with glial cells – underlying stroke pathology and recovery. Mitochondrial dysfunction has been recently recognized as a hallmark in ischemia/reperfusion neur…

0301 basic medicinelcsh:Diseases of the circulatory (Cardiovascular) systemAginglcsh:Medical technologyimpaired mitochondriavasculatureBioenergeticmedicine.medical_treatmentClinical Trials and Supportive ActivitiesIschemiaregenerative medicineReview ArticleBioenergeticsMitochondrionblood–brain barrierBioinformaticsstem cell therapycerebral ischemiaCell therapy03 medical and health sciences0302 clinical medicineClinical Researchmedicineneurovascular unitStrokeTransplantationbusiness.industryNeurosciencesGeneral MedicineStem-cell therapyblood-brain barrierStem Cell Researchmedicine.diseaseendothelial cellsBrain DisordersReview articleStrokeTransplantationtransfer of healthy mitochondria030104 developmental biologylcsh:R855-855.5lcsh:RC666-701endothelial cellStem cellbusiness030217 neurology & neurosurgeryBrain Circulation
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Elevated sodium leads to the increased expression of HSP60 and induces apoptosis in HUVECs

2017

Atherosclerosis is the leading cause of death in the world. We have previously shown that expression of heat shock protein 60 (HSP60) on the surface of endothelial cells is the main cause of initiating the disease as it acts as a T cell auto-antigen and can be triggered by classical atherosclerosis risk factors, such as infection (e.g. Chlamydia pneumoniae), chemical stress (smoking, oxygen radicals, drugs), physical insult (heat, shear blood flow) and inflammation (inflammatory cytokines, lipopolysaccharide, oxidized low density lipoprotein, advanced glycation end products). In the present study, we show that increasing levels of sodium chloride can also induce an increase in intracellular…

0301 basic medicinelcsh:MedicineApoptosisBlood PressureSodium Chloride030204 cardiovascular system & hematologyVascular MedicineHeat Shock ResponseEpitheliumUmbilical veinWhite Blood CellsSpectrum Analysis Techniques0302 clinical medicineAnimal CellsGlycationMedicine and Health Scienceslcsh:ScienceCellular Stress ResponsesMultidisciplinaryCell DeathT CellsFlow CytometryProtein TransportChemistryCell ProcessesSpectrophotometryPhysical SciencesHypertensionCytophotometryCellular TypesAnatomymedicine.symptomIntracellularResearch Articlemedicine.medical_specialtyImmune CellsSodiumImmunologychemistry.chemical_elementInflammationBiologyResearch and Analysis MethodsImmunophenotypingProinflammatory cytokine03 medical and health sciencesInternal medicineHeat shock proteinHuman Umbilical Vein Endothelial CellsmedicineHumansHeat shockBlood CellsSodiumlcsh:RChemical CompoundsBiology and Life SciencesEndothelial CellsEpithelial CellsChaperonin 60Cell BiologyAtherosclerosisBiological Tissue030104 developmental biologyEndocrinologyGene Expression RegulationchemistryImmunologySaltslcsh:QBiomarkersPLOS ONE
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MARTX Toxin in the Zoonotic Serovar of Vibrio vulnificus Triggers an Early Cytokine Storm in Mice

2017

Vibrio vulnificus biotype 2-serovar E is a zoonotic clonal complex that can cause death by sepsis in humans and fish. Unlike other biotypes, Bt2 produces a unique type of MARTXVv (Multifunctional-Autoprocessive-Repeats-in-Toxin; RtxA13), which is encoded by a gene duplicated in the pVvBt2 plasmid and chromosome II. In this work, we analyzed the activity of this toxin and its role in human sepsis by performing in vitro, ex vivo, and in vivo assays. First, we demonstrated that the ACD domain, present exclusively in this toxin variant, effectively has an actin-cross-linking activity. Second, we determined that the whole toxin caused death of human endotheliocytes and monocytes by lysis and apo…

0301 basic medicinelcsh:QR1-502MicrobiologiaVibrio vulnificusmedicine.disease_causeMonocyteslcsh:MicrobiologysepsisVibrio vulnificusCells CulturedOriginal ResearchMice Inbred BALB CCell DeathVirulencebiologyqPCR arrayInfectious DiseasesHost-Pathogen InteractionsBacteris patògensCytokinesV. vulnificusFemaleMicrobiology (medical)Virulence FactorsBacterial ToxinsImmunologyVirulenceSerogroupMicrobiologyMicrobiology03 medical and health sciencesImmune systemMARTXIn vivomedicineAnimalsHumansVibrioToxinEndothelial Cellsbiology.organism_classificationmedicine.diseaseVirologyVibrioinfectionDisease Models Animal030104 developmental biologyInfecciógene expressionCytokine stormEx vivoFrontiers in Cellular and Infection Microbiology
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