Search results for "Endothelial Cell"

showing 10 items of 497 documents

Activation of the Constitutive Androstane Receptor Inhibits Leukocyte Adhesiveness to Dysfunctional Endothelium

2021

Leukocyte cell recruitment into the vascular subendothelium constitutes an early event in the atherogenic process. As the effect of the constitutive androstane receptor (CAR) on leukocyte recruitment and endothelial dysfunction is poorly understood, this study investigated whether the role of CAR activation can affect this response and the underlying mechanisms involved. Under physiological flow conditions, TNFα-induced endothelial adhesion of human leukocyte cells was concentration-dependently inhibited by preincubation of human umbilical arterial endothelial cells with the selective human CAR ligand CITCO. CAR agonism also prevented TNFα induced VCAM-1 expression, as well as MCP-1/CCL-2 a…

MaleSmall interfering RNAEndotheliumQH301-705.5Receptors Cytoplasmic and NuclearVascular Cell Adhesion Molecule-1Leukocyte RollingRetinoid X receptorArticleendothelial dysfunctionCatalysisInorganic ChemistryMiceConstitutive androstane receptorCell AdhesionHuman Umbilical Vein Endothelial CellsLeukocytesmedicineAnimalsHumansBiology (General)Physical and Theoretical ChemistryEndothelial dysfunctionQD1-999Molecular BiologySpectroscopyconstitutive androstane receptorTumor Necrosis Factor-alphaChemistryOrganic ChemistryNF-kappa BEndothelial Cellsleukocyte recruitmentGeneral Medicinemedicine.diseaseComputer Science ApplicationsCell biologyChemistrymedicine.anatomical_structureGene Expression RegulationTumor necrosis factor alphaIntravital microscopySignal TransductionInternational Journal of Molecular Sciences
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Dynamics of complement activation in aHUS and how to monitor eculizumab therapy.

2014

Atypical hemolytic-uremic syndrome (aHUS) is associated with genetic complement abnormalities/anti–complement factor H antibodies, which paved the way to treatment with eculizumab. We studied 44 aHUS patients and their relatives to (1) test new assays of complement activation, (2) verify whether such abnormality occurs also in unaffected mutation carriers, and (3) search for a tool for eculizumab titration. An abnormal circulating complement profile (low C3, high C5a, or SC5b-9) was found in 47% to 64% of patients, irrespective of disease phase. Acute aHUS serum, but not serum from remission, caused wider C3 and C5b-9 deposits than control serum on unstimulated human microvascular endotheli…

MaleTime FactorsClinical Trials and ObservationsComplement Membrane Attack Complexurologic and male genital diseasesBiochemistryGlomerulonephritisInside BLOOD Commentaryhemic and lymphatic diseasesMembranoproliferative glomerulonephritisMonoclonalHumanizedComplement ActivationAtypical Hemolytic Uremic SyndromeEndothelial CellHematologyRemission Inductionfood and beveragesHematologyComplement C3Eculizumabmedicine.anatomical_structureFactor HFemalecomplementaHUS eculizumabmedicine.drugMembranoproliferativeHumanmedicine.medical_specialtyEndotheliumMonitoringTime FactorGlomerulonephritis MembranoproliferativeImmunologyBiologyAntibodies Monoclonal HumanizedAntibodiesInternal medicineAtypical hemolytic uremic syndromemedicineHumansPhysiologicMonitoring PhysiologicAdenosine Diphosphate RiboseEndothelial CellsCell Biologymedicine.diseaseComplement systemImmunologyAdenosine Diphosphate Ribose; Antibodies Monoclonal Humanized; Atypical Hemolytic Uremic Syndrome; Complement Activation; Complement C3; Complement Membrane Attack Complex; Endothelial Cells; Female; Glomerulonephritis Membranoproliferative; Hemolytic-Uremic Syndrome; Humans; Male; Remission Induction; Time Factors; Monitoring Physiologic; Hematology; Biochemistry; Cell Biology; ImmunologyHemolytic-Uremic SyndromeComplement membrane attack complexBlood
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Physical training and hypertension have opposite effects on endothelial brain-derived neurotrophic factor expression

2013

AIMS: Changes in circulating brain-derived neurotrophic factor (BDNF) levels were reported in patients with or at risk for cardiovascular diseases associated with endothelial dysfunction, suggesting a link between BDNF and endothelial functionality. However, little is known on cardiovascular BDNF. Our aim was to investigate levels/localization, function, and relevance of cardiovascular BDNF. METHODS AND RESULTS: BDNF levels (western blotting) and localization (immunostaining) were assessed in the heart and aorta from rats with impaired (spontaneously hypertensive rats [SHR]), normal (Wistar Kyoto rats [WKY]), and improved (SHR and WKY subjected to physical training) endothelial function. BD…

MaleTime FactorsPhysiologyAorta ThoracicRats Inbred WKYVentricular Function Left0302 clinical medicineNeurotrophic factorsRats Inbred SHRMedicineEndothelial dysfunctionCells CulturedComputingMilieux_MISCELLANEOUS0303 health sciences[SDV.BA]Life Sciences [q-bio]/Animal biologyCoronary VesselsVasodilationmedicine.anatomical_structureHypertensioncardiovascular systemCardiology and Cardiovascular Medicinemedicine.medical_specialtyCell typeEndotheliumContractility03 medical and health sciencesCoronary CirculationPhysical Conditioning AnimalPhysiology (medical)Internal medicinemedicine.arteryVentricular PressureAnimals030304 developmental biologyBrain-derived neurotrophic factorAortabusiness.industryBrain-Derived Neurotrophic FactorEndothelial Cellsmedicine.diseaseMyocardial ContractionRatsDisease Models AnimalEndocrinologynervous systemRegional Blood FlowStress Mechanicalbusiness030217 neurology & neurosurgeryImmunostaining
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Estradiol induces endothelial cell migration and proliferation through estrogen receptor-enhanced RhoA/ROCK pathway

2010

Migration and proliferation of endothelial cells are involved in re-endothelialization and angiogenesis, two important cardiovascular processes that are increased in response to estrogens. RhoA, a small GTPase which controls multiple cellular processes, is involved in the control of cell migration and proliferation. Our aim was to study the role of RhoA on estradiol-induced migration and proliferation and its dependence on estrogen receptors activity. Human umbilical vein endothelial cells were stimulated with estradiol, in the presence or absence of ICI 182780 (estrogen receptors antagonist) and Y-27632 (Rho kinase inhibitor). Estradiol increased Rho GEF-1 gene expression and RhoA (gene an…

MaleTranscriptional ActivationRHOAAngiogenesismedicine.drug_classEstrogen receptorCell Cycle ProteinsBiochemistryUmbilical CordEndocrinologyCell MovementmedicineHumansReceptorMolecular BiologyCells CulturedCell ProliferationEnzyme Assaysrho-Associated KinasesEstradiolbiologyChemistryEndothelial CellsCell migrationUp-RegulationCell biologyEndothelial stem cellReceptors EstrogenRho kinase inhibitorEstrogenCancer researchbiology.proteinFemalerhoA GTP-Binding Proteinhormones hormone substitutes and hormone antagonistsSignal TransductionMolecular and Cellular Endocrinology
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Glucocorticoid receptor knockdown decreases the antioxidant protection of B16 melanoma cells: an endocrine system-related mechanism that compromises …

2014

We previously reported an interorgan system in which stress-related hormones (corticosterone and noradrenaline), interleukin-6, and glutathione (GSH) coordinately regulate metastatic growth of highly aggressive B16-F10 melanoma cells. Corticosterone, at levels measured in tumor-bearing mice, also induces apoptotic cell death in metastatic cells with low GSH content. In the present study we explored the potential role of glucocorticoids in the regulation of metastatic cell death/survival during the early stages of organ invasion. Glucocorticoid receptor (GCR) knockdown decreased the expression and activity of γ-glutamylcysteine synthetase (γ-GCS), the rate-limiting step in GSH synthesis, in …

MaleTumor PhysiologyGlutathione reductaseCancer TreatmentMelanoma ExperimentalGene Expressionlcsh:MedicineBiochemistryAntioxidantsMetastasisAnalytical Chemistrychemistry.chemical_compoundOxidative DamageMiceGlucocorticoid receptorSpectrum Analysis TechniquesCell SignalingNeoplasmsMolecular Cell BiologyBasic Cancer ResearchMedicine and Health SciencesNeoplasm Metastasislcsh:Sciencechemistry.chemical_classificationMultidisciplinaryCell DeathGlutathione peroxidaseEndocrine TherapyFlow CytometryGlutathioneChemistrymedicine.anatomical_structureOncologyResearch DesignSpectrophotometryPhysical SciencesCytophotometryGlucocorticoidmedicine.drugResearch ArticleSignal Transductionmedicine.medical_specialtyEndotheliumClinical Research DesignCell SurvivalGlutamate-Cysteine LigaseDown-RegulationEndocrine SystemBiologyResearch and Analysis MethodsCell LineReceptors GlucocorticoidInternal medicineCell Line TumormedicineGeneticsAnimalsHumansAnimal Models of DiseaseOncogenic Signalinglcsh:RBiology and Life SciencesEndothelial CellsGlutathioneCell BiologyMice Inbred C57BLEndocrinologyHEK293 CellschemistryCell cultureCancer cellAnimal Studieslcsh:QEndothelium VascularCytometryPLoS ONE
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Suppression of the JNK Pathway by Induction of a Metabolic Stress Response Prevents Vascular Injury and Dysfunction

2008

Background— Oxidative injury and dysfunction of the vascular endothelium are early and causal features of many vascular diseases. Single antioxidant strategies to prevent vascular injury have met with mixed results. Methods and Results— Here, we report that induction of a metabolic stress response with adenosine monophosphate kinase (AMPK) prevents oxidative endothelial cell injury. This response is characterized by stabilization of the mitochondrion and increased mitochondrial biogenesis, resulting in attenuation of oxidative c-Jun N-terminal kinase (JNK) activation. We report that peroxisome proliferator coactivator 1α is a key downstream target of AMPK that is both necessary and suffici…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliumMitochondrionmedicine.disease_causeArticleMiceInternal medicinePhysiology (medical)Chlorocebus aethiopsmedicineAnimalsHumansVascular DiseasesRNA Small InterferingEndothelial dysfunctionHeat-Shock ProteinsMembrane Potential MitochondrialCell Deathbusiness.industryAdenylate KinaseJNK Mitogen-Activated Protein KinasesEndothelial CellsAMPKHydrogen PeroxideRibonucleotidesAminoimidazole CarboxamideOxidantsmedicine.diseaseAdaptation PhysiologicalPeroxisome Proliferator-Activated Receptor Gamma Coactivator 1-alphaAngiotensin IICell biologyMice Inbred C57BLEndothelial stem cellOxidative Stressmedicine.anatomical_structureEndocrinologyMitochondrial biogenesisMutagenesisCOS CellsbusinessCardiology and Cardiovascular MedicineOxidative stressTranscription FactorsCirculation
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Effects of anti-cardiolipin antibodies and IVIg on annexin A5 binding to endothelial cells: implications for cardiovascular disease

2010

Anti-phospholipid antibodies (aPL), including anti-cardiolipin antibodies (aCL), are risk factors for cardiovascular disease (CVD) in the general population and in patients with the anti-phospholipid syndrome (APS; Hughes syndrome). APS may be primary but is also common in patients with systemic lupus erythematosus (SLE). The anti-coagulant protein annexin A5 (ANXA5) is implicated in CVD by interfering with phospholipids and aPL.ANXA5 binding to human umbilical venous endothelial cells (HUVECs) was determined by flow cytometry.When cells were cultured in serum from APS patients with a high aPL titre (aPL-S), binding of ANXA5 to HUVECs was reduced. Monoclonal immunoglobulin (Ig)G aPL against…

MaleUmbilical Veinsmedicine.medical_specialtyEndotheliumPopulationImmunologyImmunoglobulin Gchemistry.chemical_compoundRheumatologyReference Valuesimmune system diseasesAntiphospholipid syndromeInternal medicineCardiolipinmedicineHumansImmunology and AllergyAnnexin A5educationneoplasmsCells CulturedProbabilityeducation.field_of_studyBinding Sitesbiologybusiness.industryEndothelial CellsImmunoglobulins IntravenousGeneral MedicineAntiphospholipid SyndromeFlow Cytometrymedicine.diseaseEndocrinologymedicine.anatomical_structurechemistryCardiovascular DiseasesAntibodies AnticardiolipinCase-Control StudiesImmunoglobulin Gbiology.proteinFemaleAnti-cardiolipin antibodiesAntibodyAnnexin A5businessScandinavian Journal of Rheumatology
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Association Between Platelet Endothelial Cellular Adhesion Molecule-1 Polymorphisms and Atherosclerosis: Results of a Study on Patients from Northern…

2010

Adhesion of circulating cells to the arterial surface is among the first detectable events in atherogenesis. Cellular adhesion molecules, expressed by the vascular endothelium and by circulating leukocytes, mediate cell recruitment and their transendothelial migration. Platelet endothelial cellular adhesion molecule-1 (PECAM-1), involved in this migration, has been associated with the development of atherosclerosis. Studies have investigated an association between coronary artery disease (CAD) and single-nucleotide polymorphisms (SNPs) located in functionally important domains of the PECAM-1 gene with inconsistent results. Thus, we have analyzed the distribution of V125L, N563S, and G670R S…

MaleUntranslated regionAgingGenotypeSingle-nucleotide polymorphismCoronary Artery DiseaseBiologyPolymorphism Single NucleotideCoronary artery diseaseGene FrequencymedicineHumansGenetic Predisposition to DiseasePlateletCell adhesionGeneAgedCell adhesion moleculeAdhesionMiddle AgedAtherosclerosismedicine.diseasePlatelet Endothelial Cell Adhesion Molecule-1ItalyCase-Control StudiesImmunologycardiovascular systemFemaleGeriatrics and GerontologyRejuvenation Research
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Vitamin D Receptor Activation Reduces Angiotensin-II–Induced Dissecting Abdominal Aortic Aneurysm in Apolipoprotein E–Knockout Mice

2015

Objective— Abdominal aortic aneurysm (AAA) is a vascular disorder characterized by chronic inflammation of the aortic wall. Low concentrations of vitamin D 3 are associated with AAA development; however, the potential direct effect of vitamin D 3 on AAA remains unknown. This study evaluates the effect of oral treatment with the vitamin D 3 receptor (VDR) ligand, calcitriol, on dissecting AAA induced by angiotensin-II (Ang-II) infusion in apoE −/− mice. Approach and Results— Oral treatment with calcitriol reduced Ang-II–induced dissecting AAA formation in apoE −/− mice, which was unrelated to systolic blood pressure or plasma cholesterol concentrations. Immunohistochemistry and reverse-tran…

MaleVascular Endothelial Growth Factor A0301 basic medicineDissecting Abdominal Aortic Aneurysm030204 cardiovascular system & hematologyLigandsCalcitriol receptorchemistry.chemical_compound0302 clinical medicineAorta AbdominalCells CulturedMice KnockoutAngiotensin IIVascular endothelial growth factorChemotaxis LeukocyteVascular endothelial growth factor APhenotypeMatrix Metalloproteinase 9Vitamin D3 ReceptorMatrix Metalloproteinase 2RNA Interferencelipids (amino acids peptides and proteins)ChemokinesMitogen-Activated Protein KinasesCardiology and Cardiovascular MedicineSignal Transductionmedicine.drugmedicine.medical_specialtyCalcitriolBiologyTransfectionProinflammatory cytokine03 medical and health sciencesApolipoproteins ECalcitriolInternal medicineHuman Umbilical Vein Endothelial CellsmedicineAnimalsHumansGenetic Predisposition to DiseaseRetinoid X Receptor alphaMacrophagesAngiotensin IIMice Inbred C57BLAortic DissectionDisease Models Animal030104 developmental biologyEndocrinologychemistryReceptors CalcitriolAortic Aneurysm AbdominalArteriosclerosis, Thrombosis, and Vascular Biology
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HIF-1α and HIF-2α Are Differentially Regulated In vivo in Neuroblastoma: High HIF-1α Correlates Negatively to Advanced Clinical Stage and Tumor Vascu…

2009

Abstract Purpose: Hypoxia is considered to be a major driving force behind tumor angiogenesis. The stabilization and activation at hypoxia of the hypoxia-inducible factors HIF-1α and HIF-2α and the concomitant induction of expression of vascular endothelial growth factor (VEGF) and other proangiogenic factors provide a molecular frame for hypoxia-driven tumor angiogenesis. This study has investigated how HIF and VEGF protein levels relate to each other with regard to vascularization, tumor stage, and overall survival in neuroblastoma. Experimental Design: Tissue cores taken from tumor specimens representing 93 children with neuroblastoma were arranged on a microarray and stained for HIF-1α,…

MaleVascular Endothelial Growth Factor ACD31Cancer ResearchPathologymedicine.medical_specialtyBiologyModels BiologicalNeovascularizationchemistry.chemical_compoundIn vivoNeoplasmsNeuroblastomaBasic Helix-Loop-Helix Transcription FactorsmedicineHumansHypoxiaRegulation of gene expressionNeovascularization PathologicInfantCancerHypoxia-Inducible Factor 1 alpha Subunitmedicine.diseaseGene Expression Regulation NeoplasticPlatelet Endothelial Cell Adhesion Molecule-1Vascular endothelial growth factorTreatment OutcomeHIF1AOncologychemistryChild PreschoolCancer researchFemalemedicine.symptomClinical Cancer Research
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