2001
Expression of vascular endothelial growth factor and its receptors is increased, but microvascular relaxation is impaired in patients after acute myocardial ischemia
Xu X, Li J, Simons M, Li J, Laham R, Sellke F. Expression of vascular endothelial growth factor and its receptors is increased, but microvascular relaxation is impaired in patients after acute myocardial ischemia. Journal Of Thoracic And Cardiovascular Surgery 2001, 121: 735-742. PMID: 11279416, DOI: 10.1067/mtc.2001.112340.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseBiomarkersBlotting, WesternCoronary Artery BypassCoronary CirculationCoronary VesselsDNA ProbesEndothelial Growth FactorsEnzyme InhibitorsFemaleGene ExpressionHeart AtriaHumansLymphokinesMaleMiddle AgedMyocardial IschemiaNitroarginineNitroprussidePrognosisProtein IsoformsReceptor Protein-Tyrosine KinasesReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorReceptors, Growth FactorReceptors, MitogenReceptors, Vascular Endothelial Growth FactorReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSubstance PVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsVasodilationVasodilator AgentsConceptsVascular endothelial growth factorEndothelial growth factorAcute myocardial ischemiaGrowth factor receptor 1Vascular endothelial growth factor receptor 1Vascular endothelial growth factor receptorFactor receptor 1Endothelial growth factor receptorMyocardial ischemiaGrowth factorReceptor 1Growth factor receptorMicrovascular relaxationFactor receptorGrowth factor receptor 2Protein expressionCoronary bypass operationsEndothelial growth factor receptor 2Vascular endothelial growth factor receptor 2Rat myocardial infarction modelFactor receptor 2Human atrial tissueVascular endothelial growthMyocardial infarction modelMessenger RNA levels
1998
Effects of coronary artery disease on expression and microvascular response to VEGF
Métais C, Li J, Li J, Simons M, Sellke F. Effects of coronary artery disease on expression and microvascular response to VEGF. American Journal Of Physiology 1998, 275: h1411-h1418. PMID: 9746492, DOI: 10.1152/ajpheart.1998.275.4.h1411.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine DiphosphateCell DivisionCoronary Artery BypassCoronary DiseaseEndothelial Growth FactorsEndothelium, VascularFemaleGene Expression RegulationGenisteinHeart AtriaHepatocyte Growth FactorHumansIn Vitro TechniquesKineticsLymphokinesMaleMicrocirculationMicroscopy, VideoMiddle AgedMuscle RelaxationMuscle, Smooth, VascularNitric Oxide SynthaseNitric Oxide Synthase Type IINitric Oxide Synthase Type IIINitroarginineProto-Oncogene ProteinsReceptor Protein-Tyrosine KinasesReceptors, Growth FactorReceptors, MitogenReceptors, Vascular Endothelial Growth FactorRNA, MessengerTranscription, GeneticVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1Vascular Endothelial Growth FactorsVasodilationConceptsCoronary artery diseaseInducible nitric oxide synthaseConstitutive nitric oxide synthaseVascular endothelial growth factorHepatocyte growth factorExpression of VEGFNitric oxide synthaseArtery diseaseNG-nitroMicrovascular responsesOxide synthaseExpression of cNOSL-arginineGrowth factorCoronary microvascular responsesSubstance P responseExogenous vascular endothelial growth factorEndothelial growth factorFlk-1 receptorFlt-1 receptorMild hypercholesterolemiaTyrosine kinase receptorsTyrosine kinase inhibitor genisteinEndothelium dysfunctionVascular responsesMyb-dependent Regulation of Thrombospondin 2 Expression ROLE OF mRNA STABILITY*
Bein K, Ware J, Simons M. Myb-dependent Regulation of Thrombospondin 2 Expression ROLE OF mRNA STABILITY*. Journal Of Biological Chemistry 1998, 273: 21423-21429. PMID: 9694906, DOI: 10.1074/jbc.273.33.21423.Peer-Reviewed Original ResearchConceptsNIH 3T3 cellsC-MybWild-type NIH 3T3 cellsTranscription factor c-MybEndogenous target genesPost-transcriptional mechanismsPromoter-reporter assaysMRNA stability studiesDifferential display analysisSimilar transcriptional levelsTSP-2 expressionV-SrcHomology searchCDNA endsGene productsTarget genesTranscriptional levelMRNA stabilityV-mycCell cycleTSP-1C-JunHematopoietic cellsDNA probesHomologous products
1997
Macrophage-dependent regulation of syndecan gene expression.
Li J, Brown L, Laham R, Volk R, Simons M. Macrophage-dependent regulation of syndecan gene expression. Circulation Research 1997, 81: 785-96. PMID: 9351452, DOI: 10.1161/01.res.81.5.785.Peer-Reviewed Original ResearchConceptsBlood-derived macrophagesSyndecan expressionSyndecan geneMyocardial infarctionGene expressionRegulation of expressionSyndecan-1Op/op miceGranulocyte-macrophage colony-stimulating factorMacrophage colony-stimulating factorRat infarct modelColony-stimulating factorHeparin-binding growth factorsSyndecan-4 mRNASyndecan-1 mRNABiological processesMacrophage influxCellular responsesMacrophage contentSyndecan-4Right ventricleTissue injuryOp miceExtracellular matrixPrompt increaseAntisense oligonucleotide inhibition of PDGFR-beta receptor subunit expression directs suppression of intimal thickening.
Sirois M, Simons M, Edelman E. Antisense oligonucleotide inhibition of PDGFR-beta receptor subunit expression directs suppression of intimal thickening. Circulation 1997, 95: 669-76. PMID: 9024156, DOI: 10.1161/01.cir.95.3.669.Peer-Reviewed Original Research
1993
Relation between Activated Smooth-Muscle Cells in Coronary-Artery Lesions and Restenosis after Atherectomy
Simons M, Leclerc G, Safian R, Isner J, Weir L, Baim D. Relation between Activated Smooth-Muscle Cells in Coronary-Artery Lesions and Restenosis after Atherectomy. New England Journal Of Medicine 1993, 328: 608-613. PMID: 8429852, DOI: 10.1056/nejm199303043280903.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsMyosin heavy chainNonmuscle myosin heavy chainRecurrent luminal narrowingCoronary artery lesionsExercise thallium scintigraphyVascular smooth muscle cellsCoronary atherosclerotic plaquesPresence of restenosisHigh-power fieldGroup of lesionsNegative resultsAngiographic followCoronary atherectomyCoronary angioplastyThallium scintigraphyCoronary lesionsLuminal narrowingNeointimal proliferationSubsequent restenosisLate lossLuminal diameterHeavy chainHigh riskAtherectomy
1992
Antisense c-myb oligonucleotides inhibit intimal arterial smooth muscle cell accumulation in vivo
Simons M, Edelman E, DeKeyser J, Langer R, Rosenberg R. Antisense c-myb oligonucleotides inhibit intimal arterial smooth muscle cell accumulation in vivo. Nature 1992, 359: 67-70. PMID: 1522889, DOI: 10.1038/359067a0.Peer-Reviewed Original Research