2001
PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation
Bao J, Sato K, Li M, Gao Y, Abid R, Aird W, Simons M, Post M. PR-39 and PR-11 peptides inhibit ischemia-reperfusion injury by blocking proteasome-mediated IκBα degradation. AJP Heart And Circulatory Physiology 2001, 281: h2612-h2618. PMID: 11709430, DOI: 10.1152/ajpheart.2001.281.6.h2612.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Bacterial AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHumansI-kappa B ProteinsIntercellular Adhesion Molecule-1MaleMultienzyme ComplexesMyocardial Reperfusion InjuryMyocardiumNADPH OxidasesNeutrophilsNF-KappaB Inhibitor alphaPeptide FragmentsPeroxidasePhosphoproteinsProteasome Endopeptidase ComplexRatsRats, Sprague-DawleyReactive Oxygen SpeciesUmbilical VeinsVascular Cell Adhesion Molecule-1Ventricular Function, LeftConceptsIschemia-reperfusion injuryB alpha degradationAdhesion molecule-1PR-11Alpha degradationNeutrophil infiltrationMyeloperoxidase activityInfarct sizeMolecule-1Vascular cell adhesion molecule-1Myocardial ischemia-reperfusion injuryIntercellular adhesion molecule-1Cell adhesion molecule-1Ventricular systolic pressureTime of reperfusionIschemia-reperfusion modelMin of ischemiaPR-39Controls 24 hBlood pressureSystolic pressureCardiac functionIntramyocardial injectionIκBα degradationAdhesion moleculesSerotonin-induced human coronary microvascular contraction during acute myocardial ischemia is blocked by COX-2 inhibition
Métais C, Bianchi C, Li J, Li J, Simons M, Sellke F. Serotonin-induced human coronary microvascular contraction during acute myocardial ischemia is blocked by COX-2 inhibition. Basic Research In Cardiology 2001, 96: 59-67. PMID: 11215533, DOI: 10.1007/s003950170078.Peer-Reviewed Original ResearchMeSH KeywordsAgedCoronary VesselsCyclooxygenase 1Cyclooxygenase 2Cyclooxygenase 2 InhibitorsCyclooxygenase InhibitorsFemaleHeart AtriaHumansIsoenzymesMaleMembrane ProteinsMicrocirculationMiddle AgedMyocardial IschemiaMyocardiumNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroprussideProstaglandin-Endoperoxide SynthasesSerotoninSubstance PVasoconstrictionConceptsAcute myocardial ischemiaMyocardial ischemiaContractile responseCoronary arteriolesPotent contractile responseAcute coronary syndromeCOX-2 expressionCOX-2 inhibitionCOX-2 mRNAMicrovascular contractionSNP relaxationCoronary spasmCoronary syndromeL-NNACardiac surgeryAtherosclerotic patientsSubstance PNOS-2Prostaglandin releaseCOX-1IschemiaAtrial tissueSodium nitroprussideNOS-3Prostacyclin synthase
1999
Angiogenesis in Cardiovascular Disease
Sellke F, Simons M. Angiogenesis in Cardiovascular Disease. Drugs 1999, 58: 391-396. PMID: 10493268, DOI: 10.2165/00003495-199958030-00001.Peer-Reviewed Original ResearchConceptsInoperable coronary artery diseaseTherapeutic angiogenesisChronic myocardial ischaemiaCoronary artery diseasePreliminary clinical trialsAngiogenic growth factorsMyocardial revascularisationArtery diseaseMyocardial ischaemiaTreatment optionsGrowth factor proteinClinical trialsCardiovascular diseaseMyocardial perfusionProtein administrationAnimal modelsAngiogenic factorsObjective evidenceGrowth factorAngiogenesisPatientsDiseaseAdministrationGene therapyOptimal candidatesMyocyte-dependent Regulation of Endothelial Cell Syndecan-4 Expression ROLE OF TNF-α*
Zhang Y, Pasparakis M, Kollias G, Simons M. Myocyte-dependent Regulation of Endothelial Cell Syndecan-4 Expression ROLE OF TNF-α*. Journal Of Biological Chemistry 1999, 274: 14786-14790. PMID: 10329676, DOI: 10.1074/jbc.274.21.14786.Peer-Reviewed Original ResearchConceptsSyndecan-4 expressionECV cellsProtein kinase C alphaCardiac myocytesGene familySyndecan-4 mRNATNF-alphaPosttranscriptional mechanismsGene expressionPrimary cardiac myocytesUnique memberC alphaHuman endothelial cellsSyndecan-4Western analysisMouse cardiac myocytesSyndecan-4 levelsNormal myoblastsDependent mannerNF-kappaBExpressionH9c2 cellsHypoxic conditionsTumor necrosisEndothelial cellsEffect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig
Tofukuji M, Metais C, Collard C, Morse D, Stahl G, Nelson D, Li J, Simons M, Sellke F. Effect of sialyl Lewisx oligosaccharide on myocardial and cerebral injury in the pig. The Annals Of Thoracic Surgery 1999, 67: 112-119. PMID: 10086534, DOI: 10.1016/s0003-4975(98)01130-8.Peer-Reviewed Original ResearchConceptsArtery blood flowCardiopulmonary bypassMyeloperoxidase activityBrain arteriolesNeutrophil infiltrationOrgan perfusionBlood flowInducible isoformInternal carotid artery blood flowEndothelium-dependent relaxation responsesCoronary artery blood flowCarotid artery blood flowLeft ventricular systolic pressureNitric oxide synthase mRNAAdministration of CYBeneficial acute effectsCerebral vascular resistanceEndothelium-independent relaxationEndothelium-dependent relaxationVentricular systolic pressureCoronary artery occlusionMyocardial contractile functionNormothermic cardiopulmonary bypassLeft ventricular pressureNitric oxide synthase
1995
Magnetic resonance mapping demonstrates benefits of VEGF–induced myocardial angiogenesis
Pearlman J, Hibberd M, Chuang M, Harada K, Lopez J, Gladstone S, Friedman M, Sellke F, Simons M. Magnetic resonance mapping demonstrates benefits of VEGF–induced myocardial angiogenesis. Nature Medicine 1995, 1: 1085-1089. PMID: 7489368, DOI: 10.1038/nm1095-1085.Peer-Reviewed Original ResearchConceptsVascular endothelial growth factorMagnetic resonance imagingBlood supplyCoronary occlusive diseasePlacebo-controlled studyCollateral blood supplyBetter ejection fractionCoronary artery occlusionCause of deathCollateral vessel developmentEndothelial growth factorRegional wall thickeningArtery occlusionOcclusive diseaseEjection fractionCollateral vesselsCoronary arteryCollateral developmentIschemic zoneVEGF infusionMyocardial angiogenesisResonance imagingWall thickeningHeart attackPorcine model