2016
Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1&bgr; Production
Ceneri N, Zhao L, Young BD, Healy A, Coskun S, Vasavada H, Yarovinsky TO, Ike K, Pardi R, Qin L, Qin L, Tellides G, Hirschi K, Meadows J, Soufer R, Chun HJ, Sadeghi M, Bender JR, Morrison AR. Rac2 Modulates Atherosclerotic Calcification by Regulating Macrophage Interleukin-1&bgr; Production. Arteriosclerosis Thrombosis And Vascular Biology 2016, 37: 328-340. PMID: 27834690, PMCID: PMC5269510, DOI: 10.1161/atvbaha.116.308507.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaAortic DiseasesApolipoproteins EAtherosclerosisCells, CulturedCoronary Artery DiseaseCoronary VesselsFemaleGenetic Predisposition to DiseaseHumansInflammation MediatorsInterleukin 1 Receptor Antagonist ProteinInterleukin-1betaMacrophagesMaleMice, Inbred C57BLMice, KnockoutMuscle, Smooth, VascularMyocytes, Smooth MuscleNeuropeptidesPhenotypePlaque, AtheroscleroticPrognosisRac GTP-Binding ProteinsRac1 GTP-Binding ProteinSignal TransductionTransfectionUp-RegulationVascular CalcificationConceptsCoronary calcium burdenIL-1β expressionCalcium burdenSerum IL-1β levelsElevated IL-1βIL-1β levelsCoronary artery diseaseInterleukin-1β expressionCalcified coronary arteryCardiovascular deathCardiovascular eventsArtery diseaseIndependent predictorsClinical outcomesVascular calcificationCoronary arteryIL-1βPlaque calciumAtherosclerotic calcificationExperimental atherogenesisInflammatory regulatorsMacrophage interleukinAtherosclerotic plaquesTherapeutic targetProgressive calcification
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
2004
Simvastatin Modulates Angiotensin II Signaling Pathway by Preventing Rac1-Mediated Upregulation of p27
ZENG L, XU H, CHEW TL, CHISHOLM R, SADEGHI MM, KANWAR YS, DANESH FR. Simvastatin Modulates Angiotensin II Signaling Pathway by Preventing Rac1-Mediated Upregulation of p27. Journal Of The American Society Of Nephrology 2004, 15: 1711-1720. PMID: 15213258, DOI: 10.1097/01.asn.0000129839.91567.68.Peer-Reviewed Original ResearchMeSH KeywordsActive Transport, Cell NucleusAngiotensin IIAnimalsBlotting, WesternCell Cycle ProteinsCell LineCyclin-Dependent Kinase Inhibitor p27Hydrogen PeroxideHydroxymethylglutaryl-CoA Reductase InhibitorsLeucineMicroscopy, ConfocalModels, BiologicalOxidation-ReductionPhosphorylationProtein Serine-Threonine KinasesProto-Oncogene ProteinsProto-Oncogene Proteins c-aktRac1 GTP-Binding ProteinRatsSignal TransductionSimvastatinTransfectionTumor Suppressor ProteinsUp-RegulationConceptsP27 protein expressionAng IIAng II stimulationIntracellular H2O2 productionModulatory effectsMesangial cellsProtein expressionII stimulationCyclin-dependent kinase inhibitor p27P27 proteinEffect of simvastatinCell cycle levelSmall GTPAkt kinaseH2O2 productionRat mesangial cellsCholesterol-lowering propertiesAddition of mevalonateLipid attachmentDownstream activationRac1 activitySignaling pathwaysAkt activationIsoprenoid intermediatesGeranylgeranyl pyrophosphate
2002
3-Hydroxy-3-methylglutaryl CoA reductase inhibitors prevent high glucose-induced proliferation of mesangial cells via modulation of Rho GTPase/ p21 signaling pathway: Implications for diabetic nephropathy
Danesh FR, Sadeghi MM, Amro N, Philips C, Zeng L, Lin S, Sahai A, Kanwar YS. 3-Hydroxy-3-methylglutaryl CoA reductase inhibitors prevent high glucose-induced proliferation of mesangial cells via modulation of Rho GTPase/ p21 signaling pathway: Implications for diabetic nephropathy. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 8301-8305. PMID: 12048257, PMCID: PMC123062, DOI: 10.1073/pnas.122228799.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCell DifferentiationCell MembraneCells, CulturedCyclin-Dependent Kinase Inhibitor p21Cyclin-Dependent KinasesCyclinsDiabetic NephropathiesDNA ReplicationEnzyme InhibitorsGlomerular MesangiumGlucoseHydroxymethylglutaryl-CoA Reductase InhibitorsModels, BiologicalProtein PrenylationProtein TransportRatsRho GTP-Binding ProteinsSignal TransductionSimvastatinTransfectionConceptsDiabetic nephropathyMesangial cellsP21 protein expressionProtein expressionCdk2 kinase activityReductase inhibitorsExposure of MCsHigh glucose-induced proliferationProliferation of MCsUse of statinsHMG-CoA reductase inhibitorsLipid-lowering agentsCoronary heart diseaseCholesterol-lowering effectCoA reductase inhibitorsGlucose-induced proliferationGlomerular mesangial cellsRat mesangial cellsCholesterol-lowering propertiesStatin therapyHeart diseaseClinical dataCell cycle levelMC proliferationHigh glucose