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
2000
Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide
Gao Y, Lecker S, Post M, Hietaranta A, Li J, Volk R, Li M, Sato K, Saluja A, Steer M, Goldberg A, Simons M. Inhibition of ubiquitin-proteasome pathway–mediated IκBα degradation by a naturally occurring antibacterial peptide. Journal Of Clinical Investigation 2000, 106: 439-448. PMID: 10930447, PMCID: PMC314329, DOI: 10.1172/jci9826.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnti-Infective AgentsAntimicrobial Cationic PeptidesCells, CulturedCysteine EndopeptidasesDNA-Binding ProteinsGene ExpressionHumansI-kappa B ProteinsMaleMiceMice, Inbred ICRMice, TransgenicMultienzyme ComplexesMyocardial InfarctionNF-kappa BNF-KappaB Inhibitor alphaPancreatitisPeptidesProteasome Endopeptidase ComplexSwineUbiquitinsConceptsDependent gene expressionGene expressionNF-kappa BUbiquitin-proteasome pathwayB alpha phosphorylationValosin-containing proteinB alpha degradationNF-kappa B inhibitor ICellular functionsTranscription factorsAlpha phosphorylationBiological processesInhibitor IAlpha 7 subunitSelective regulationProteasome activityB alphaAntibacterial peptidesOverall proteasome activityAlpha degradationNF-kappaBCell culturesIκBα degradationExpressionPeptidesPR39, a peptide regulator of angiogenesis
Li J, Post M, Volk R, Gao Y, Li M, Metais C, Sato K, Tsai J, Aird W, Rosenberg R, Hampton T, Li J, Sellke F, Carmeliet P, Simons M. PR39, a peptide regulator of angiogenesis. Nature Medicine 2000, 6: 49-55. PMID: 10613823, DOI: 10.1038/71527.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntimicrobial Cationic PeptidesAortaCapillariesCattleCell HypoxiaCells, CulturedCoronary VesselsCysteine EndopeptidasesDNA-Binding ProteinsEndothelium, VascularHeartHumansHypoxia-Inducible Factor 1Hypoxia-Inducible Factor 1, alpha SubunitIn Vitro TechniquesMacrophagesMiceMice, Inbred C57BLMice, TransgenicMultienzyme ComplexesMyocardial InfarctionMyocardial IschemiaNeovascularization, PhysiologicNuclear ProteinsPeptidesProteasome Endopeptidase ComplexRecombinant ProteinsSwineTranscription FactorsUbiquitinsUmbilical VeinsVon Willebrand FactorConceptsHypoxia-inducible factor-1α (HIF-1α) degradationMacrophage-derived peptideHypoxia-inducible factor-1α (HIF-1α) proteinCoronary flow studiesInflammation-induced angiogenesisInduction of angiogenesisMyocardial vasculatureTissue injuryPotent inductorFunctional blood vesselsBlood vesselsVascular structuresAngiogenesisSelective inhibitionPR39