Featured Publications
Syndecan 4 is required for endothelial alignment in flow and atheroprotective signaling
Baeyens N, Mulligan-Kehoe MJ, Corti F, Simon DD, Ross TD, Rhodes JM, Wang TZ, Mejean CO, Simons M, Humphrey J, Schwartz MA. Syndecan 4 is required for endothelial alignment in flow and atheroprotective signaling. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 17308-17313. PMID: 25404299, PMCID: PMC4260558, DOI: 10.1073/pnas.1413725111.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAtherosclerosisBlotting, WesternCells, CulturedEndothelial CellsFemaleHuman Umbilical Vein Endothelial CellsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMice, Inbred C57BLMice, KnockoutMicroscopy, ConfocalNF-kappa BReverse Transcriptase Polymerase Chain ReactionRNA InterferenceSignal TransductionStress, MechanicalSyndecan-4Vascular Endothelial Growth Factor Receptor-2ConceptsHuman umbilical vein endothelial cellsNF-κBProinflammatory NF-κBAtherosclerotic plaque burdenKruppel-like factor 2Umbilical vein endothelial cellsVEGF receptor 2Appearance of plaquesVein endothelial cellsHypercholesterolemic micePlaque burdenAntiinflammatory pathwayThoracic aortaReceptor 2Endothelial cellsEndothelial alignmentFlow correlatesCausal roleAtherosclerosisFactor 2MiceCyclic stretchLocalization correlatesActivationSyndecan-4
2018
Bradykinin B2 Receptor Contributes to Inflammatory Responses in Human Endothelial Cells by the Transactivation of the Fibroblast Growth Factor Receptor FGFR-1
Terzuoli E, Corti F, Nannelli G, Giachetti A, Donnini S, Ziche M. Bradykinin B2 Receptor Contributes to Inflammatory Responses in Human Endothelial Cells by the Transactivation of the Fibroblast Growth Factor Receptor FGFR-1. International Journal Of Molecular Sciences 2018, 19: 2638. PMID: 30200598, PMCID: PMC6163484, DOI: 10.3390/ijms19092638.Peer-Reviewed Original ResearchConceptsFibroblast growth factor receptor 1Human umbilical vein endothelial cellsCell permeabilityEndothelial cellsFGFR-1 phosphorylationEndothelial cell permeabilityFGF-2 signalingFGF-2 pathwaysFGF-2/FGFRFGFR-1 inhibitorsC-SrcGrowth factor receptor 1Umbilical vein endothelial cellsDownstream signalingHuman endothelial cellsGrowth factor 2Vein endothelial cellsFactor receptor 1Cell migrationFGF-2 upregulationAmplification loopSignalingFactor 2Angiogenic disordersBradykinin B2 receptorPeptides derived from the histidine–proline rich glycoprotein bind copper ions and exhibit anti-angiogenic properties
Magrì A, Grasso G, Corti F, Finetti F, Greco V, Santoro AM, Sciuto S, La Mendola D, Morbidelli L, Rizzarelli E. Peptides derived from the histidine–proline rich glycoprotein bind copper ions and exhibit anti-angiogenic properties. Dalton Transactions 2018, 47: 9492-9503. PMID: 29963662, DOI: 10.1039/c8dt01560k.Peer-Reviewed Original ResearchConceptsElectron paramagnetic resonanceCircular dichroismSpray ionization mass spectrometryPotential drug delivery systemElectron spray ionization mass spectrometryMeans of potentiometryIonization mass spectrometryDrug delivery systemsAmidic bondCopper ionsRole of copperParamagnetic resonanceMass spectrometryComplex speciesTrehalose derivativesProdrug systemEnzymatic degradationDelivery systemCopperPeptidesPotentiometryBondsUVSpectrometryDichroism
2010
Interaction between Sensory C-fibers and Cardiac Mast Cells in Ischemia/Reperfusion: Activation of a Local Renin-Angiotensin System Culminating in Severe Arrhythmic Dysfunction
Morrey C, Brazin J, Seyedi N, Corti F, Silver RB, Levi R. Interaction between Sensory C-fibers and Cardiac Mast Cells in Ischemia/Reperfusion: Activation of a Local Renin-Angiotensin System Culminating in Severe Arrhythmic Dysfunction. Journal Of Pharmacology And Experimental Therapeutics 2010, 335: 76-84. PMID: 20668055, PMCID: PMC2957783, DOI: 10.1124/jpet.110.172262.Peer-Reviewed Original ResearchMeSH KeywordsAldehydesAnimalsArrhythmias, CardiacBeta-N-AcetylhexosaminidasesCalcitonin Gene-Related PeptideCell DegranulationCells, CulturedFluorescent Antibody TechniqueGuinea PigsIn Vitro TechniquesMaleMast CellsMyocardial Reperfusion InjuryMyocardiumNerve EndingsNerve Fibers, UnmyelinatedNorepinephrineReninRenin-Angiotensin SystemSensory Receptor CellsSubstance PSynaptosomesConceptsRenin-angiotensin systemIschemia/reperfusionCardiac mast cellsSubstance P receptor blockadeLocal renin-angiotensin systemSubstance PMast cellsSensory nervesCultured mast cellsRenin releaseReceptor blockadeCardiac dysfunctionLocal cardiac renin-angiotensin systemCardiac renin-angiotensin systemCardiac nerve terminalsCardiac sensory nervesMast cell reninSubstance P releaseSensory C-fibersMast cell stabilizationSubstance P receptorCardiac synaptosomesReperfusion arrhythmiasNorepinephrine overflowAngiotensin production
2008
Dutch and arctic mutant peptides of β amyloid1–40 differentially affect the FGF-2 pathway in brain endothelium
Solito R, Corti F, Fossati S, Mezhericher E, Donnini S, Ghiso J, Giachetti A, Rostagno A, Ziche M. Dutch and arctic mutant peptides of β amyloid1–40 differentially affect the FGF-2 pathway in brain endothelium. Experimental Cell Research 2008, 315: 385-395. PMID: 19061884, PMCID: PMC2764262, DOI: 10.1016/j.yexcr.2008.11.002.Peer-Reviewed Original ResearchConceptsAnti-angiogenic profileDegree of tropismCerebral amyloid angiopathyFGF-2 expressionFGF-2 receptorFibroblast growth factorEndothelial cell proliferationMicrovessel remodelingAmyloid angiopathyBrain endotheliumΒ-amyloid1Brain vesselsInduction of apoptosisAbeta variantsCerebral ECsFGF-2 pathwaysG variantE22GGrowth factorWT peptideFGFR-1Cell proliferationFGF-2Hereditary phenotypesDifferential effects