2014
Fibroblast growth factor receptor 1 is a key inhibitor of TGFβ signaling in the endothelium
Chen PY, Qin L, Tellides G, Simons M. Fibroblast growth factor receptor 1 is a key inhibitor of TGFβ signaling in the endothelium. Science Signaling 2014, 7: ra90. PMID: 25249657, DOI: 10.1126/scisignal.2005504.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell TransdifferentiationCoronary VesselsEndothelium, VascularExtracellular MatrixFibroblastsGraft RejectionHeart TransplantationHeterograftsHindlimbHuman Umbilical Vein Endothelial CellsHumansIschemiaMesodermMiceMice, Mutant StrainsMicroRNAsMuscle, Smooth, VascularNeointimaReceptor, Fibroblast Growth Factor, Type 1Receptors, Fibroblast Growth FactorSignal TransductionSmad2 ProteinTransforming Growth Factor betaTransplantation ChimeraConceptsFibroblast growth factor receptor 1Growth factor receptor 1Factor receptor 1Extracellular matrixSmooth muscle cellsMuscle cellsEndothelial cell-specific knockoutKey regulatorReceptor 1TGFβ signalingCell-specific knockoutDecreased abundanceMesenchymal transitionKey inhibitorVascular homeostasisGrowth factorDevelopment of EndMTRecurrence of stenosisTGFβGrowth of neointimaCellsNeointima formationEndMTVascular lumenSignaling
2013
Endothelial Cell–Dependent Regulation of Arteriogenesis
Moraes F, Paye J, Mac Gabhann F, Zhuang ZW, Zhang J, Lanahan AA, Simons M. Endothelial Cell–Dependent Regulation of Arteriogenesis. Circulation Research 2013, 113: 1076-1086. PMID: 23897694, PMCID: PMC3865810, DOI: 10.1161/circresaha.113.301340.Peer-Reviewed Original ResearchConceptsAdult arteriogenesisCell-autonomous fashionGrowth factor signalingMouse linesCell-autonomous effectsKnockin mouse lineMorphogenetic defectsArterial morphogenesisCell type-specific deletionFactor signalingCell typesCre-driver mouse linesSynectinAttractive therapeutic strategyOcclusive atherosclerotic diseaseMuscle cellsEndothelial cellsRegulationArterial conduitsAtherosclerotic diseaseTherapeutic strategiesAdult miceClinical importanceArteriogenesisCells
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 responsesPhosphorylation of the Cytoplasmic Tail of Syndecan-4 Regulates Activation of Protein Kinase Cα*
Horowitz A, Simons M. Phosphorylation of the Cytoplasmic Tail of Syndecan-4 Regulates Activation of Protein Kinase Cα*. Journal Of Biological Chemistry 1998, 273: 25548-25551. PMID: 9748216, DOI: 10.1074/jbc.273.40.25548.Peer-Reviewed Original Research
1997
c-Myb-dependent cell cycle progression and Ca2+ storage in cultured vascular smooth muscle cells.
Husain M, Bein K, Jiang L, Alper S, Simons M, Rosenberg R. c-Myb-dependent cell cycle progression and Ca2+ storage in cultured vascular smooth muscle cells. Circulation Research 1997, 80: 617-26. PMID: 9130442, DOI: 10.1161/01.res.80.5.617.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsCultured vascular smooth muscle cellsSmooth muscle cellsCell cycle progressionMuscle cellsCycle progressionCell populationsC-myb expressionC-MybReleasable Ca2G1/S interfaceCytoplasmic Ca2C-Myb activityGrowth factorCell clonesCell proliferationProgressionSignificant reductionStable cell clonesProto-oncogeneTransient inductionC-myb proto-oncogeneS-phase entryCa2Growth-arrested cellsAntisense 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
1996
…and surreal antisense?
Simons M, Rosenberg R, Edelman E. …and surreal antisense? Nature Medicine 1996, 2: 131-132. PMID: 8574948, DOI: 10.1038/nm0296-131b.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