2013
Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis
Nie L, Guo X, Esmailzadeh L, Zhang J, Asadi A, Collinge M, Li X, Kim JD, Woolls M, Jin SW, Dubrac A, Eichmann A, Simons M, Bender JR, Sadeghi MM. Transmembrane protein ESDN promotes endothelial VEGF signaling and regulates angiogenesis. Journal Of Clinical Investigation 2013, 123: 5082-5097. PMID: 24177422, PMCID: PMC3859420, DOI: 10.1172/jci67752.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDBlood VesselsCadherinsCells, CulturedEar, ExternalEndothelium, VascularHindlimbHuman Umbilical Vein Endothelial CellsHumansIschemiaMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutNeovascularization, PhysiologicNeuropilinsProtein Tyrosine Phosphatase, Non-Receptor Type 1Protein Tyrosine Phosphatase, Non-Receptor Type 2Retinal VesselsRNA InterferenceRNA, Small InterferingVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2ZebrafishZebrafish ProteinsConceptsSmooth muscle cell-derived neuropilin-like proteinAberrant blood vessel formationNormal vascular developmentProtein tyrosineTC-PTPTransmembrane proteinTherapeutic targetBlood vessel formationVEGF responseNegative regulatorDevelopmental angiogenesisVEGFR-2Vascular developmentAttractive therapeutic targetESDNAngiogenesis regulationVE-cadherinVessel formationEC proliferationComplex formationRegulatorProteinNeuropilin expressionVEGF receptorsEndothelial VEGF
2010
VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling
Zhang J, Silva T, Yarovinsky T, Manes TD, Tavakoli S, Nie L, Tellides G, Pober JS, Bender JR, Sadeghi MM. VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling. Circulation Research 2010, 107: 408-417. PMID: 20538685, PMCID: PMC2929975, DOI: 10.1161/circresaha.109.210963.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedArteriesBevacizumabCD3 ComplexCoronary VesselsHumansJurkat CellsLymphocytesMiceMice, SCIDReceptors, Vascular Endothelial Growth FactorT-LymphocytesTransplantation, HeterologousVascular Endothelial Growth Factor AConceptsVascular endothelial growth factorRole of VEGFAdhesion molecule-1T cellsVascular remodelingHuman T cellsMolecule-1Recombinant intercellular adhesion molecule-1Human arteriesVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cell adhesion molecule-1Inhibition of VEGFT cell accumulationPeripheral blood mononuclearEffects of VEGFSubpopulation of CD3Novel therapeutic approachesEndothelial growth factorT cell activationT cell linesVEGFR-1 mRNAT cell captureLymphocyte recruitmentBlood mononuclear
2006
HMG-CoA reductase inhibitor simvastatin mitigates VEGF-induced “inside-out” signaling to extracellular matrix by preventing RhoA activation
Xu H, Zeng L, Peng H, Chen S, Jones J, Chew TL, Sadeghi MM, Kanwar YS, Danesh FR. HMG-CoA reductase inhibitor simvastatin mitigates VEGF-induced “inside-out” signaling to extracellular matrix by preventing RhoA activation. American Journal Of Physiology. Renal Physiology 2006, 291: f995-f1004. PMID: 16774905, DOI: 10.1152/ajprenal.00092.2006.Peer-Reviewed Original ResearchMeSH KeywordsActin CytoskeletonActinsAnimalsCells, CulturedCollagen Type IVExtracellular MatrixFocal Adhesion Protein-Tyrosine KinasesHydroxymethylglutaryl-CoA Reductase InhibitorsIntegrin beta1Mesangial CellsMevalonic AcidPhosphorylationProlineRatsRhoA GTP-Binding ProteinSignal TransductionSimvastatinTritiumTyrosineVascular Endothelial Growth Factor AConceptsRhoA activationIntact actin cytoskeletonCell signaling cascadesPrecise signaling mechanismUnderlying molecular mechanismsActin cytoskeletonECM expansionMevalonate depletionSignaling cascadesIntegrin activationMevalonate pathwayECM accumulationMolecular mechanismsVEGF stimulationSignaling mechanismComplex biologyExtracellular matrixPleiotropic effectsAngiogenic polypeptideType IV collagen accumulationEndothelial cell permeabilityExtracellular matrix accumulationCell permeabilityGrowth factorPathological processes
2005
HMG CoA reductase inhibition modulates VEGF‐induced endothelial cell hyperpermeability by preventing RhoA activation and myosin regulatory light chain phosphorylation
Zeng L, Xu H, Chew T, Eng E, Sadeghi MM, Adler S, Kanwar YS, Danesh FR. HMG CoA reductase inhibition modulates VEGF‐induced endothelial cell hyperpermeability by preventing RhoA activation and myosin regulatory light chain phosphorylation. The FASEB Journal 2005, 19: 1845-1847. PMID: 16160062, DOI: 10.1096/fj.05-4240fje.Peer-Reviewed Original ResearchMeSH KeywordsActinsAnimalsBlotting, WesternCell LineCytoplasmCytoskeletonCytosolDiabetic NephropathiesElectric ImpedanceEndothelial CellsEndothelium, VascularGreen Fluorescent ProteinsHydroxymethylglutaryl CoA ReductasesHydroxymethylglutaryl-CoA Reductase InhibitorsKidney GlomerulusMevalonic AcidMicroscopy, ConfocalModels, BiologicalModels, StatisticalMyosin Light ChainsPermeabilityPhosphorylationRatsRhoA GTP-Binding ProteinSignal TransductionSimvastatinTransfectionVascular Endothelial Growth Factor A