2018
Galectin‐3 exacerbates ox‐LDL‐mediated endothelial injury by inducing inflammation via integrin β1‐RhoA‐JNK signaling activation
Chen X, Lin J, Hu T, Ren Z, Li L, Hameed I, Zhang X, Men C, Guo Y, Xu D, Zhan Y. Galectin‐3 exacerbates ox‐LDL‐mediated endothelial injury by inducing inflammation via integrin β1‐RhoA‐JNK signaling activation. Journal Of Cellular Physiology 2018, 234: 10990-11000. PMID: 30536538, PMCID: PMC6590151, DOI: 10.1002/jcp.27910.Peer-Reviewed Original ResearchMeSH KeywordsAtherosclerosisCell Adhesion MoleculesCell SurvivalEndothelium, Vascularfas ReceptorGalectin 3Gene Expression RegulationHuman Umbilical Vein Endothelial CellsHumansInflammationIntegrin beta1JNK Mitogen-Activated Protein KinasesLipoproteins, LDLMAP Kinase Signaling SystemrhoA GTP-Binding ProteinConceptsHuman umbilical vascular endothelial cellsEndothelial injuryGal-3P-JNKInflammatory factorsGTP-RhoAGalectin-3Plasma galectin-3Systemic inflammatory disorderEndothelial cell injuryPathogenesis of atherosclerosisLow-density lipoproteinNF-κB activationVascular endothelial cellsEndothelial dysfunctionP-IKKβAS patientsInflammatory disordersP-p65P-IKKαCardiovascular diseaseOx-LDLCell injuryCCK8 assayControl groupA novel method for segmenting growth of cells in sheared endothelial culture reveals the secretion of an anti-inflammatory mediator
Ghim M, Pang K, Arshad M, Wang X, Weinberg P. A novel method for segmenting growth of cells in sheared endothelial culture reveals the secretion of an anti-inflammatory mediator. Journal Of Biological Engineering 2018, 12: 15. PMID: 30127849, PMCID: PMC6092814, DOI: 10.1186/s13036-018-0107-6.Peer-Reviewed Original ResearchVascular cell adhesion molecule-1Intercellular adhesion molecule-1Adhesion molecule-1Molecule-1Cell adhesion molecule-1Anti-inflammatory mediatorsAnti-inflammatory effectsPathogenesis of atherosclerosisEndothelial cellsBlood vesselsNormal physiologyEndothelial culturesGrowth of cellsMediatorsConclusionsThe resultsEndotheliumNon-coding RNA regulation of endothelial and macrophage functions during atherosclerosis
Aryal B, Suárez Y. Non-coding RNA regulation of endothelial and macrophage functions during atherosclerosis. Vascular Pharmacology 2018, 114: 64-75. PMID: 29551552, PMCID: PMC6177333, DOI: 10.1016/j.vph.2018.03.001.Peer-Reviewed Original ResearchConceptsNon-coding RNAsNon-coding RNA regulationSmall non-coding RNAsMultiple cell functionsRNA regulationMacrophage functionRNA moleculesGene expressionPotential regulatorKey playersVascular biologyPathogenesis of atherosclerosisCell functionSpecific roleLncRNAsRegulationRNAMechanism of actionEndothelial cellsInitial eventVascular integrityRecruitment of monocytesMicroRNAsDevelopment of atherosclerosisBiology
2017
Shear Stress Induces Change in Extracellular Signal-Regulated Kinase 5 Levels with Sustained Activation under Disturbed and Continuous Laminar Flow
Shalaby SY, Chitragari G, Sumpio BJ, Sumpio BE. Shear Stress Induces Change in Extracellular Signal-Regulated Kinase 5 Levels with Sustained Activation under Disturbed and Continuous Laminar Flow. International Journal Of Angiology 2017, 26: 109-115. PMID: 28566937, PMCID: PMC5446257, DOI: 10.1055/s-0037-1599057.Peer-Reviewed Original ResearchExtracellular signal-regulated kinase 5Pathogenesis of atherosclerosisExposure of HUVECERK5 activationVascular dysfunctionPattern of activationFro flowVascular remodelingConfluent HUVECsHours of exposurePhospho-ERK5Endothelial integrityActivation of ERK5Kinase 5Sustained activationEnd of experimentationERK5 phosphorylationHUVECActivationHoursExposureTransient phosphorylationCell lysatesDisturbed flow conditionsParallel plate flow chamber
2016
Inflammatory cytokines in atherosclerosis: current therapeutic approaches
Tousoulis D, Oikonomou E, Economou EK, Crea F, Kaski JC. Inflammatory cytokines in atherosclerosis: current therapeutic approaches. European Heart Journal 2016, 37: 1723-1732. PMID: 26843277, DOI: 10.1093/eurheartj/ehv759.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsChronic inflammatory diseaseCurrent therapeutic approachesPathogenesis of atherosclerosisRole of cytokinesCardiovascular disease progressionTreatment of atherosclerosisPotential clinical significanceSmooth muscle cellsInflammatory cascadeInflammatory cytokinesInflammatory diseasesDisease progressionClinical significanceTherapeutic approachesAtherosclerotic plaquesColchicine actAtherosclerosisMuscle cellsCytokinesTypes of cellsSpecific antibodiesKey moleculesMultiple effectsCellsStatins
2015
The role of microRNAs in coronary artery disease: From pathophysiology to diagnosis and treatment
Economou EK, Oikonomou E, Siasos G, Papageorgiou N, Tsalamandris S, Mourouzis K, Papaioanou S, Tousoulis D. The role of microRNAs in coronary artery disease: From pathophysiology to diagnosis and treatment. Atherosclerosis 2015, 241: 624-633. PMID: 26117399, DOI: 10.1016/j.atherosclerosis.2015.06.037.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsMeSH KeywordsAnimalsApoptosisAtherosclerosisBiomarkersBlood PlateletsCell MovementCoronary Artery DiseaseDisease ProgressionEndothelium, VascularGene Expression RegulationHumansLipoproteins, HDLLipoproteins, LDLMiceMicroRNAsMonocytesMuscle, Smooth, VascularMyocardial InfarctionNeovascularization, PathologicOligonucleotidesReperfusion InjuryStem CellsConceptsCoronary artery diseaseDevelopment of atherosclerosisArtery diseaseCoronary artery disease progressionPathogenesis of atherosclerosisStudy of miRNAsMyocardial infarctionDisease progressionSpecific miRNA expression patternsTherapeutic approachesRole of microRNAsPreventive opportunitiesDiagnostic biomarkersRelated conditionsAtherosclerosisMiRNA expression patternsDiseaseNon-coding RNA moleculesRole of miRNAsIntercellular communicationIntracellular regulatorsExpression patternsMiRNAsPost-transcriptional levelGene expressionEndothelial Glucocorticoid Receptor Suppresses Atherogenesis—Brief Report
Goodwin JE, Zhang X, Rotllan N, Feng Y, Zhou H, Fernández-Hernando C, Yu J, Sessa WC. Endothelial Glucocorticoid Receptor Suppresses Atherogenesis—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2015, 35: 779-782. PMID: 25810297, PMCID: PMC4375730, DOI: 10.1161/atvbaha.114.304525.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisBody WeightBrachiocephalic TrunkCholesterolDiet, High-FatDisease Models, AnimalEndothelial CellsGenotypeMacrophagesMice, Inbred C57BLMice, KnockoutPhenotypeReceptors, GlucocorticoidSeverity of Illness IndexTime FactorsTriglyceridesConceptsEndothelial glucocorticoid receptorGlucocorticoid receptorHigh-fat diet feedingApoE knockout backgroundSevere atherosclerotic lesionsGroups of micePathogenesis of atherosclerosisAortic sinusTotal cholesterolAtherosclerosis progressionBrachiocephalic arteryControl miceInflammatory milieuTonic inhibitionDiet feedingMacrophage recruitmentAtherosclerotic lesionsBody weightMiceKnockout backgroundReceptorsLesionsAtherosclerosisInflammationArteryThe Role and Predictive Value of Cytokines in Atherosclerosis and Coronary Artery Disease.
Tousoulis D, Economou EK, Oikonomou E, Papageorgiou N, Siasos G, Latsios G, Kokkou E, Mourouzis K, Papaioannou S, Deftereos S, Cleman MW, Lymberi M, Gennimata V, Stefanadis C. The Role and Predictive Value of Cytokines in Atherosclerosis and Coronary Artery Disease. Current Medicinal Chemistry 2015, 22: 2636-50. PMID: 25876746, DOI: 10.2174/0929867322666150415145814.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsCoronary artery diseaseArtery diseaseChronic inflammatory diseasePathogenesis of atherosclerosisRole of cytokinesProcess of atherogenesisSmooth muscle cellsPrognostic significanceInflammatory diseasesAtherosclerotic plaquesPredictive valueAtherosclerosisCytokinesMuscle cellsTypes of cellsDiseaseMultiple effectsCellsCurrent informationInflammationAtherogenesisPathogenesisLeukocytesPlaques
2014
Effect of Pulsatile and Continuous Flow on Yes-Associated Protein
Chitragari G, Shalaby SY, Sumpio BJ, Sumpio BE. Effect of Pulsatile and Continuous Flow on Yes-Associated Protein. International Journal Of Angiology 2014, 23: 183-186. PMID: 25317030, PMCID: PMC4169103, DOI: 10.1055/s-0034-1376865.Peer-Reviewed Original ResearchHuman umbilical vein endothelial cellsContinuous forward flowTotal YAPPhosphorylated YAPEndothelial cellsPathogenesis of atherosclerosisEffects of pulsatileRole of YAPUmbilical vein endothelial cellsVein endothelial cellsYes-Associated ProteinMild decreaseFlow chamber systemFibronectin-coated glass slidesParallel plate flow chamber systemSignificant decreaseLonger durationSignificant differencesAtherosclerosisDifferential effectsLevel of phosphorylationForward flowMinutesYAPPFF
2013
Connective tissue growth factor induces osteogenic differentiation of vascular smooth muscle cells through ERK signaling
HUANG J, HUANG H, WU M, LI J, XIE H, ZHOU H, LIAO E, PENG Y. Connective tissue growth factor induces osteogenic differentiation of vascular smooth muscle cells through ERK signaling. International Journal Of Molecular Medicine 2013, 32: 423-429. PMID: 23722620, DOI: 10.3892/ijmm.2013.1398.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBiomarkersCalcification, PhysiologicCell TransdifferentiationConnective Tissue Growth FactorCore Binding Factor Alpha 1 SubunitExtracellular Signal-Regulated MAP KinasesGene Expression RegulationMiceMuscle, Smooth, VascularMyocytes, Smooth MuscleOsteocytesOsteogenesisSignal TransductionConceptsConnective tissue growth factorTissue growth factorVSMC calcificationRole of CTGFSmooth muscle specific αGrowth factorCalcification of VSMCsVascular smooth muscle cell growthVascular smooth muscle cellsSmooth muscle cell growthPathogenesis of atherosclerosisMouse thoracic aortaSmooth muscle cellsMuscle cell growthERK-specific inhibitorAlkaline phosphataseVascular calcificationExtracellular signal-regulated kinase (ERK) activityThoracic aortaVSMC transdifferentiationBone markersAlizarin Red S stainingTranscription factor 2Primary VSMCsMuscle cells
2010
6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle
Martin K, Rzucidlo E, Ding M, Merenick B, Kasza Z, Wagner R, Powell R. 6.05 In Vitro Vascular Cell Culture Systems – Vascular Smooth Muscle. 2010, 69-96. DOI: 10.1016/b978-0-08-046884-6.00705-3.ChaptersVascular smooth muscle cellsPhenotypic modulationInsulin-like growth factor IEndothelial cellsVSMC differentiationPathogenesis of atherosclerosisRapamycin (mTOR) inhibitor rapamycinSerum response factorDedifferentiated vascular smooth muscle cellsGrowth factor INormal vascular physiologyActivated T cellsSmooth muscle cellsContractile protein expressionEffects of drugsT cellsSmooth muscleIntimal hyperplasiaFactor family membersTumor angiogenesisVascular physiologyMature arteriesFactor IMuscle cellsVSMC phenotype
2009
Paricalcitol (19-nor-1,25-dihydroxyvitamin D2) and calcitriol (1,25-dihydroxyvitamin D3) exert potent immunomodulatory effects on dendritic cells and inhibit induction of antigen-specific T cells
Sochorová K, Budinský V, Rožková D, Tobiasová Z, Dusilová-Sulková S, Špíšek R, Bartůňková J. Paricalcitol (19-nor-1,25-dihydroxyvitamin D2) and calcitriol (1,25-dihydroxyvitamin D3) exert potent immunomodulatory effects on dendritic cells and inhibit induction of antigen-specific T cells. Clinical Immunology 2009, 133: 69-77. PMID: 19660988, DOI: 10.1016/j.clim.2009.06.011.Peer-Reviewed Original ResearchConceptsAntigen-specific T cellsDendritic cellsT cellsVDR agonistsImmunomodulatory effectsChronic immune-mediated inflammatory diseaseEnd-stage renal disease patientsImmune-mediated inflammatory diseasesImmunomodulatory activityVitamin D receptor activatorsRenal disease patientsImmature dendritic cellsRisk of atherosclerosisPathogenesis of atherosclerosisPotent immunomodulatory effectsToll-like receptorsBioactive IL-12Functional TregsIL-12DC differentiationCalcium resorptionDisease patientsHypercalcemic effectInflammatory diseasesImmunomodulatory potency
2007
Regulation of vascular smooth muscle cell differentiation
Rzucidlo E, Martin K, Powell R. Regulation of vascular smooth muscle cell differentiation. Journal Of Vascular Surgery 2007, 45: a25-a32. PMID: 17544021, DOI: 10.1016/j.jvs.2007.03.001.Peer-Reviewed Reviews, Practice Guidelines, Standards, and Consensus StatementsConceptsVascular smooth muscle cell differentiationSmooth muscle cell differentiationMuscle cell differentiationCell differentiationPathogenesis of atherosclerosisMajor human diseasesLocal environmental cuesEnvironmental cuesContractile roleIntimal hyperplasiaDifferentiated stateVascular aneurysmsMolecular mechanismsVascular developmentPhenotypic switchingHuman diseasesVessel wallVSMCCritical roleDifferentiationEssential componentHypertensionAsthmaAtherosclerosisHyperplasia
2003
Shear stress stimulated endothelial cell derived PDGF and IL-1 alpha both stimulate SMC chemotaxis via the MAPK pathway
Dardik A, Yamashita A, Aziz F, Paszkowiak J, Asada H, Sumpio B. Shear stress stimulated endothelial cell derived PDGF and IL-1 alpha both stimulate SMC chemotaxis via the MAPK pathway. Journal Of Surgical Research 2003, 114: 249. DOI: 10.1016/j.jss.2003.08.159.Peer-Reviewed Original ResearchPlatelet-derived growth factor-BBIL-1SMC migrationEndothelial cellsMAPK inhibitor PD98059Pathogenesis of atherosclerosisSMC chemotaxisSmooth muscle cell migrationIL-1 alphaInterleukin-1 alphaSimilar degreeInhibitor PD98059Muscle cell migrationMAPK pathwayHemodynamic forcesGrowth factor-BBAortic endothelial cellsSS stimulationBovine aortic endothelial cellsArterial levelsNeointimal hyperplasiaParacrine mechanismsSMC mitogenBoyden chamberSoluble factorsTissue factor pathway inhibitors as a novel approach to antithrombotic therapy.
Sajadi S, Ezekowitz MD, Dhond A, Netrebko P. Tissue factor pathway inhibitors as a novel approach to antithrombotic therapy. Drug News & Perspectives 2003, 16: 363-9. PMID: 12973447, DOI: 10.1358/dnp.2003.16.6.829308.Peer-Reviewed Original ResearchConceptsTissue factor pathway inhibitorFactor pathway inhibitorTissue factorPathway inhibitorNew antithrombotic approachComplications of atherosclerosisPathogenesis of atherosclerosisAntithrombotic therapyAntithrombotic approachEndothelial injurySystemic hemostasisNeointimal formationVascular interventionsAtherosclerotic plaquesEndothelial cellsInhibitory effectExtrinsic pathwayAtherosclerosisInhibitorsPlaquesCoagulationEarly stagesComplicationsFactorsAnticoagulants
2001
Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect
Seli E, Selam B, Mor G, Kayisli U, Pehlivan T, Arici A. Estradiol regulates monocyte chemotactic protein-1 in human coronary artery smooth muscle cells: a mechanism for its antiatherogenic effect. Menopause The Journal Of The North American Menopause Society 2001, 8: 296-301. PMID: 11449089, DOI: 10.1097/00042192-200107000-00013.Peer-Reviewed Original ResearchConceptsHuman coronary artery smooth muscle cellsCoronary artery smooth muscle cellsArtery smooth muscle cellsMonocyte chemotactic protein-1Smooth muscle cellsChemotactic protein-1Recruitment of macrophagesMCP-1 expressionMCP-1 proteinMuscle cellsProtective effectProtein 1Arterial wallSelective estrogen receptor modulatorsCoronary smooth muscle cellsMCP-1 protein productionEstrogen's protective effectPhenol red-free mediumCharcoal-stripped calf serumProtein productionEstrogen receptor modulatorsPathogenesis of atherosclerosisReverse transcriptase-polymerase chain reactionNorthern blotLow-density lipoprotein
1998
Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL
Calvo D, Gómez-Coronado D, Suárez Y, Lasunción M, Vega M. Human CD36 is a high affinity receptor for the native lipoproteins HDL, LDL, and VLDL. Journal Of Lipid Research 1998, 39: 777-788. PMID: 9555943, DOI: 10.1016/s0022-2275(20)32566-9.Peer-Reviewed Original ResearchConceptsHigh-affinity receptorHuman CD36Lipoprotein HDLAffinity receptorPathogenesis of atherosclerosisLow-density lipoproteinFoam cell formationBinding of lipoproteinsFatty acid metabolismSR-BIActive fatty acid metabolismDensity lipoproteinModified lipoproteinsScavenger receptorsLipid metabolismCD36CLA-1Monoclonal antibodiesLDLLipoproteinHDLAcid metabolismReceptorsVLDLNative lipoproteins
1996
The role of advanced glycosylation end-products in the pathogenesis of atherosclerosis
Makita Z, Yanagisawa K, Kuwajima S, Bucala R, Vlassara H, Koike T. The role of advanced glycosylation end-products in the pathogenesis of atherosclerosis. Nephrology Dialysis Transplantation 1996, 11: 31-33. PMID: 9044304, DOI: 10.1093/ndt/11.supp5.31.Peer-Reviewed Original ResearchConceptsEnd-stage renal diseaseLow-density lipoproteinDiabetic patientsDevelopment of atherosclerosisAGE-LDLAdvanced glycosylationAGE-modified formCoronary artery diseaseSerum total cholesterolPathogenesis of atherosclerosisArtery diseaseDiabetes mellitusRenal diseaseTotal cholesterolCerebrovascular diseaseMarked elevationRapid progressionTissue injuryVascular pathologyNormal controlsPatientsAGE-modified peptidesAtherogenic formAtherosclerosisAGE modification
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