Search results for "Endothelial Cell"

showing 10 items of 497 documents

Fluvastatin stabilizes the blood–brain barrier in vitro by nitric oxide-dependent dephosphorylation of myosin light chains

2006

Inhibition of the 3-hydroxy-3-methylglutaryl-coenzyme-A reductase and the downstream mevalonate pathway is in part responsible for the beneficial effects that statins exert on the cardiovascular system. In this study we aimed at analysing the stabilizing effects of fluvastatin on the blood-brain barrier (BBB) integrity, using an in vitro co-culture model of ECV304 and C6, or primary bovine endothelial cells and rat astrocytes. Fluvastatin dose-dependently (1-25 micromol/l) increased barrier integrity as analysed by measurements of transendothelial electrical resistance (TEER). This effect (117.4+/-2.6% at 25 micromol/l) was significantly reduced by the nitric oxide (NO) synthase inhibitor L…

IndolesMyosin Light ChainsMyosin light-chain kinaseGeranylgeranyl pyrophosphatePhosphataseFarnesyl pyrophosphateBiologyNitric OxideBlood–brain barrierAntioxidantsCapillary PermeabilityFatty Acids MonounsaturatedDephosphorylationMiceCellular and Molecular Neurosciencechemistry.chemical_compoundElectric ImpedancemedicineAnimalsDrug InteractionsEnzyme InhibitorsFluvastatinCells CulturedPharmacologyAnalysis of VarianceMicroscopy Confocalomega-N-MethylarginineDose-Response Relationship DrugEndothelial CellsBiological TransportMolecular biologyCoculture TechniquesRatsmedicine.anatomical_structurechemistryBiochemistryBlood-Brain BarrierAstrocytesModels AnimalCattleMevalonate pathwayFluvastatinmedicine.drugNeuropharmacology
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Fluvastatin prevents glutamate-induced blood-brain-barrier disruption in vitro.

2008

Abstract Glutamate is an important excitatory amino acid in the central nervous system. Under pathological conditions glutamate levels dramatically increase. Aim of the present study was to examine whether the HMG-CoA inhibitor fluvastatin prevents glutamate-induced blood-brain-barrier (BBB) disruption. Measurements of transendothelial electrical resistance (TEER) were performed to analyze BBB integrity in an in vitro co-culture model of brain endothelial and glial cells. Myosin light chain (MLC) phosphorylation was detected by immunohistochemistry, or using the in-cell western technique. Intracellular Ca 2+ and reactive oxygen species (ROS) levels were analyzed using the fluorescence dyes …

IndolesMyosin Light ChainsTime FactorsIntracellular SpaceGlutamic AcidBiologymedicine.disease_causeNitric OxideReceptors N-Methyl-D-AspartateGeneral Biochemistry Genetics and Molecular BiologyNitric oxideCell LineFatty Acids Monounsaturatedchemistry.chemical_compoundBAPTAmedicineElectric ImpedanceAnimalsGeneral Pharmacology Toxicology and PharmaceuticsPhosphorylationFluvastatinDose-Response Relationship DrugGlutamate receptorEndothelial CellsGeneral MedicineCell biologyRatsOxidative StresschemistryBiochemistryBlood-Brain BarrierApocyninNMDA receptorCalciumNAD+ kinaseReactive Oxygen SpeciesOxidative stressFluvastatinmedicine.drugSignal TransductionLife sciences
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Host–pathogen interactions in Vibrio vulnificus: responses of monocytes and vascular endothelial cells to live bacteria

2015

ABSTRACT  Aim: To demonstrate that Vibrio vulnificus, a sepsis-related aquatic pathogen, can provoke a strong pro-inflammatory reaction in blood-associated target cells. Materials & methods: We selected two strains of the two main phylogenetic lineages, two human cell lines, monocytes and vascular endothelial cells and designed an in vitro infection model simulating early septicemia. Results: Both strains caused a strong cell-specific pro-inflammatory response and produced a high degree of cell damage that ended with death by lysis (endothelial cells) or apoptosis/lysis (monocytes). The interaction with endothelial cells was stronger than expected and significantly different for both l…

InflammationMicrobiology (medical)LysisbiologyGene Expression ProfilingEndothelial CellsVibrio vulnificusbiology.organism_classificationmedicine.diseaseMicrobiologyVirologyMonocytesIn vitroMicrobiologySepsisStress PhysiologicalApoptosisHost-Pathogen InteractionsmedicineHumansVibrio vulnificusPathogenCell damageCells CulturedBacteriaFuture Microbiology
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Timing effect of intramyocardial hydrogel injection for positively impacting left ventricular remodeling after myocardial infarction

2015

Intramyocardial injection of various injectable hydrogel materials has shown benefit in positively impacting the course of left ventricular (LV) remodeling after myocardial infarction (MI). However, since LV remodeling is a complex, time dependent process, the most efficacious time of hydrogel injection is not clear. In this study, we injected a relatively stiff, thermoresponsive and bioabsorbable hydrogel in rat hearts at 3 different time points - immediately after MI (IM), 3 d post-MI (3D), and 2 w post-MI (2W), corresponding to the beginnings of the necrotic, fibrotic and chronic remodeling phases. The employed left anterior descending coronary artery ligation model showed expected infar…

InjectionTime FactorsMacrophageMyocardial InfarctionInfarction02 engineering and technology030204 cardiovascular system & hematologyCardiac tissue engineeringAntigens CD31Hydrogel Polyethylene Glycol DimethacrylateHeart Ventricle0302 clinical medicineFibrosisMyocardial infarctionInflammation MediatorVentricular RemodelingIntervention timing021001 nanoscience & nanotechnologyPlatelet Endothelial Cell Adhesion Molecule-1Neutrophil InfiltrationMechanics of MaterialsSelf-healing hydrogelsCardiologyCytokinesFemalemedicine.symptomInflammation Mediators0210 nano-technologymedicine.medical_specialtyMaterials scienceTime FactorHeart VentriclesBiophysicsInflammationBioengineeringCeramics and CompositeAnterior Descending Coronary ArteryArticleInjectionsBiomaterials03 medical and health sciencesInternal medicinemedicineAnimalsMechanics of MaterialVentricular remodelingCytokineActinAnimalMacrophagesMyocardiummedicine.diseaseBiomaterialInjectable materialActinsHydrogelRats Inbred LewCeramics and CompositesLigation
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Functionality of endothelial cells on silk fibroin nets: Comparative study of micro- and nanometric fibre size

2007

Biomimetic material design, such as mimicking nanostructured components of the extracellular matrix, is an actual challenge for biomaterial research with a high impact on tissue engineering and regenerative medicine. Thus, understanding the cellular response at the cell biological and molecular level and the consequences of various chemically or physically modified biomaterials is highly important. In the present study we assessed the response of human umbilical vein endothelial cells (HUVEC) and outgrowth endothelial cells (OEC) from endothelial progenitor cells to different variants of nanofibrous silk fibroin nets in comparison to microfibrous silk fibroin scaffolds with regard to cellul…

IntegrinsMaterials scienceBiophysicsFibroinBioengineeringBiomaterialsExtracellular matrixFocal adhesionTissue engineeringSpectroscopy Fourier Transform InfraredCell AdhesionAnimalsHumansNanotopographyAmino AcidsCell adhesionCell ShapeCells CulturedChromatography High Pressure LiquidCell adhesion moleculefungiEndothelial CellsAdhesionBombyxNanostructuresMechanics of MaterialsMicroscopy Electron ScanningCeramics and CompositesBiophysicsFibroinsBiomedical engineeringBiomaterials
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Cross-talk between minimally primed HL-60 cells and resting HUVEC reveals a crucial role for adhesion over extracellularly released oxidants

2011

This study demonstrates that a long-lasting co-culture of neutrophil surrogates (HL-60 cells), minimally primed by platelet activating factor (PAF), and resting endothelial cells (EC) results in the elaboration of an hyper-adhesive endothelial surface, as measured by the increase in the expression of endothelial adhesion molecules E-Selectin, VCAM-1, and ICAM-1. This endothelial dysfunction is mediated by the activation of the redox-sensitive transcription factor NF-κB through an exclusive adhesion-driven mechanism active in the endothelial cell: reactive oxygen and nitrogen species, extracellularly released by minimally primed HL-60 cells, are not involved in the induction of the endotheli…

Intercellular Adhesion Molecule-1Vascular Cell Adhesion Molecule-1HL-60 CellsInflammationNeutrophils Priming Endothelial cells Inflammation Adhesion Oxidants.BiologyBiochemistryCell Linechemistry.chemical_compoundSettore BIO/10 - BiochimicaE-selectinCell AdhesionmedicineHumansEndothelial dysfunctionCell adhesionPharmacologyPlatelet-activating factorCell adhesion moleculeNF-kappa BEndothelial CellsReceptor Cross-TalkIntercellular Adhesion Molecule-1Oxidantsmedicine.diseaseCoculture TechniquesCell biologyEndothelial stem cellchemistrybiology.proteinmedicine.symptomE-SelectinReactive Oxygen SpeciesBiochemical Pharmacology
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Acute endothelial failure after cosmetic iris implants (NewIris®)

2011

We report a case of an acute endothelial failure after the implantation of a new cosmetic, colored, artificial iris diaphragm implant called NewIris(®). A 21-year-old woman came to us complaining of progressive loss of vision and pain after NewIris lenses had been implanted. Decreased visual acuity, corneal edema, and increased intraocular pressure in both eyes appeared only 3 weeks after the surgery. The lenses were removed as soon as possible but had already severely affected the endothelial cell count. NewIris implants are an alternative to cosmetic contact lenses, but they are not as safe as other phakic anterior chamber intraocular lenses, nor are they a good option for the patient.

Intraocular pressuremedicine.medical_specialtygenetic structuresbusiness.industryCase Reportendothelial failureNewIrisEndothelial cell counteye diseasescosmetic iris implantsSurgeryOphthalmologymedicine.anatomical_structureCorneal edemaIntraocular lensesOphthalmologyDecreased Visual AcuitymedicineImplantsense organsIris (anatomy)businessClinical Ophthalmology (Auckland, N.Z.)
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Correction: Oncogenic extracellular HSP70 disrupts the gap-junctional coupling between capillary cells

2021

High levels of circulating heat shock protein 70 (HSP70) are detected in many cancers. In order to explore the effects of extracellular HSP70 on human microvascular endothelial cells (HMEC), we initially used gap-FRAP technique. Extracellular human HSP70 (rhHSP70), but not rhHSP27, blocks the gap-junction intercellular communication (GJIC) between HMEC, disrupts the structural integrity of HMEC junction plaques, and decreases connexin43 (Cx43) expression, which correlates with the phosphorylation of Cx43 serine residues. Further exploration of these effects identified a rapid transactivation of the Epidermal Growth Factor Receptor in a Toll-Like Receptor 4-dependent manner, preceding its in…

Junctional couplingChemistryCapillary actionCorrectionEndothelial CellsGap JunctionsCell CommunicationRecombinant ProteinsHsp70OncologyConnexin 43BiophysicsExtracellularHumansHSP70 Heat-Shock ProteinsPhosphorylationOncotarget
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Effect of boldine, secoboldine, and boldine methine on angiotensin II-induced neutrophil recruitment in vivo.

2005

AbstractAngiotensin-II (Ang-II) has inflammatory activity and is involved in different diseases associated with the cardiovascular system. This study has evaluated the effect of boldine (B), and two phenanthrene alkaloids semisynthesized by us, secoboldine (SB) and boldine methine (BM), on Ang-II-induced neutrophil recruitment. Intraperitoneal administration of 1 nM Ang-II induced significant neutrophil accumulation, which was maximal at 4–8 h. BM inhibited neutrophil infiltration into the peritoneal cavity at 4 h and 8 h by 73% and 77%, respectively, SB at 8 h by 55%, and B had no effect on this response. Although BM inhibited the release of cytokine-inducible neutrophil chemoattractant/ke…

KeratinocytesMaleChemokineAporphinesEndotheliumNeutrophilsImmunologyChemokine CXCL2InflammationPharmacologyRats Sprague-Dawleychemistry.chemical_compoundIn vivomedicineImmunology and AllergyBoldineAnimalsHumansInfusions ParenteralPlatelet Activating FactorReceptorchemistry.chemical_classificationReactive oxygen speciesbiologyMolecular StructureAngiotensin IIMonokinesInterleukin-8Endothelial CellsCell BiologyPhenanthrenesAngiotensin IIRatsP-Selectinmedicine.anatomical_structureBiochemistrychemistrybiology.proteinIntercellular Signaling Peptides and Proteinsmedicine.symptomChemokinesReactive Oxygen SpeciesChemokines CXCJournal of leukocyte biology
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Unsaturated Fatty Acids Drive Disintegrin and Metalloproteinase (ADAM)-dependent Cell Adhesion, Proliferation, and Migration by Modulating Membrane F…

2011

The disintegrin-metalloproteinases ADAM10 and ADAM17 mediate the release of several cell signaling molecules and cell adhesion molecules such as vascular endothelial cadherin or L-selectin affecting endothelial permeability and leukocyte transmigration. Dysregulation of ADAM activity may contribute to the pathogenesis of vascular diseases, but the mechanisms underlying the control of ADAM functions are still incompletely understood. Atherosclerosis is characterized by lipid plaque formation and local accumulation of unsaturated free fatty acids (FFA). Here, we show that unsaturated FFA increase ADAM-mediated substrate cleavage. We demonstrate that these alterations are not due to genuine ch…

KeratinocytesMembrane FluidityADAM10Lipid BilayersVascular permeabilityBiologyADAM17 ProteinBiochemistryCapillary PermeabilityADAM10 ProteinCell MovementMembrane fluidityCell AdhesionAnimalsHumansCell adhesionMolecular BiologyCell ProliferationCell adhesion moleculeCell growthFluorescence recovery after photobleachingEndothelial CellsMembrane ProteinsCell BiologyAtherosclerosisADAM ProteinsCell biologyLipoproteins LDLADAM ProteinsHEK293 CellsFatty Acids UnsaturatedCholesterol EstersRabbitsAmyloid Precursor Protein SecretasesGranulocytes
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