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 molecules
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 increaseRat arterial wall retains myointimal hyperplastic potential long after arterial injury.
Sirois M, Simons M, Kuter D, Rosenberg R, Edelman E. Rat arterial wall retains myointimal hyperplastic potential long after arterial injury. Circulation 1997, 96: 1291-8. PMID: 9286961, DOI: 10.1161/01.cir.96.4.1291.Peer-Reviewed Original ResearchConceptsSmooth muscle cellsVascular diseaseNeointimal hyperplasiaMuscle cellsMedial smooth muscle cellsBlood vesselsAccelerated vascular diseaseSingle-dose therapyPDGFR-beta expressionVascular smooth muscle cellsPlatelet-derived growth factorProliferative vascular diseasesPeriod of thrombocytopeniaArterial injuryEndothelial denudationVascular injuryPlatelet depletionIntimal hyperplasiaPharmacological modalitiesVascular healingArterial wallHyperplasiaGrowth factorNative vesselsInjuryAntisense 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
1995
c-myc in Vasculoproliferative Disease
Edelman E, Simons M, Sirois M, Rosenberg R. c-myc in Vasculoproliferative Disease. Circulation Research 1995, 76: 176-182. PMID: 7834827, DOI: 10.1161/01.res.76.2.176.Peer-Reviewed Original Research