2013
NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth
Jaba IM, Zhuang ZW, Li N, Jiang Y, Martin KA, Sinusas AJ, Papademetris X, Simons M, Sessa WC, Young LH, Tirziu D. NO triggers RGS4 degradation to coordinate angiogenesis and cardiomyocyte growth. Journal Of Clinical Investigation 2013, 123: 1718-1731. PMID: 23454748, PMCID: PMC3613910, DOI: 10.1172/jci65112.Peer-Reviewed Original ResearchMeSH KeywordsAdaptation, BiologicalAnimalsCell EnlargementCells, CulturedCoronary VesselsEndothelium, VascularHeart VentriclesMechanistic Target of Rapamycin Complex 1MiceMice, Inbred C57BLMice, TransgenicMultiprotein ComplexesMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterNitric OxideNitric Oxide SynthasePlacenta Growth FactorPregnancy ProteinsProteinsProteolysisProto-Oncogene Proteins c-aktRatsRats, Sprague-DawleyRGS ProteinsSignal TransductionTOR Serine-Threonine KinasesConceptsCardiomyocyte growthAkt/mTORC1 signalingNovel NO-dependent mechanismProteasomal degradationCoordination of angiogenesisMTORC1 signalingConditional overexpressionMurine cardiac tissueG proteinsTransgenic expressionAkt/Physiological mechanismsMyocyte growthVessel growthGrowth factorTransgenic miceHypertrophic responseAngiogenesisKnockout miceMyocardial hypertrophyExpressionGrowthCardiac hypertrophyNOS inhibitor L-NAMEInduction
2007
Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice
Tirziu D, Chorianopoulos E, Moodie KL, Palac RT, Zhuang ZW, Tjwa M, Roncal C, Eriksson U, Fu Q, Elfenbein A, Hall AE, Carmeliet P, Moons L, Simons M. Myocardial hypertrophy in the absence of external stimuli is induced by angiogenesis in mice. Journal Of Clinical Investigation 2007, 117: 3188-3197. PMID: 17975666, PMCID: PMC2045601, DOI: 10.1172/jci32024.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenic ProteinsAnimalsCardiomegalyCells, CulturedEchocardiographyEndothelial CellsEnzyme InhibitorsHeartHemodynamicsMiceMice, Inbred C57BLMice, TransgenicMyocardiumMyocytes, CardiacNeovascularization, PhysiologicNG-Nitroarginine Methyl EsterOrgan SizeRatsRats, Sprague-DawleyTransgenesConceptsMyocardial hypertrophyHeart sizeNormal heart sizeENOS inhibitor L-NAMEInhibitor L-NAMEAtrial natriuretic factorHypertrophic marker expressionNormal adult mouse heartAdult mouse heartAngiogenic growth factorsL-NAMEBeta-MHCCardiac massMyocardial infarctionMyocardial functionNatriuretic factorCardiac performanceCardiomyocyte sizeTransgenic miceStimulation periodHeart growthHypertrophy markersMarker expressionMouse heartsMurine heartProtection against myocardial ischemia-reperfusion injury by the angiogenic Masterswitch protein PR 39 gene therapy: the roles of HIF1alpha stabilization and FGFR1 signaling.
Muinck ED, Nagy N, Tirziu D, Murakami M, Gurusamy N, Goswami SK, Ghatpande S, Engelman RM, Simons M, Das DK. Protection against myocardial ischemia-reperfusion injury by the angiogenic Masterswitch protein PR 39 gene therapy: the roles of HIF1alpha stabilization and FGFR1 signaling. Antioxidants & Redox Signaling 2007, 9: 437-45. PMID: 17280485, DOI: 10.1089/ars.2006.1501.Peer-Reviewed Original ResearchMeSH KeywordsAdenoviridaeAnimalsAntimicrobial Cationic PeptidesApoptosisBlotting, WesternCell LineGenetic TherapyHumansHypoxia-Inducible Factor 1, alpha SubunitIn Situ Nick-End LabelingMaleMalondialdehydeMiceMice, Inbred C57BLMutationMyocardial Reperfusion InjuryReactive Oxygen SpeciesReceptor, Fibroblast Growth Factor, Type 1Signal TransductionTime FactorsConceptsCoronary flowMyocardial ischemic reperfusion injuryMyocardial ischemia-reperfusion injuryEmpty vectorIschemia-reperfusion injuryIschemic reperfusion injuryLVdP/dtVentricular developed pressureMin of ischemiaBaseline coronary flowMyocardial infarct sizeGene therapyReperfusion injuryCardioprotective abilityInfarct sizeDeveloped pressureHIF-1alpha proteinTTC stainingAortic flowHeart rateCardiomyocyte apoptosisEx vivoCardioprotectionHIF1alpha stabilizationHemodynamics