2016
miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart
Li N, Hwangbo C, Jaba IM, Zhang J, Papangeli I, Han J, Mikush N, Larrivée B, Eichmann A, Chun HJ, Young LH, Tirziu D. miR-182 Modulates Myocardial Hypertrophic Response Induced by Angiogenesis in Heart. Scientific Reports 2016, 6: 21228. PMID: 26888314, PMCID: PMC4758045, DOI: 10.1038/srep21228.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCardiomegalyEndotheliumMechanistic Target of Rapamycin Complex 1Membrane ProteinsMiceMice, KnockoutMicroRNAsMultiprotein ComplexesMyocytes, CardiacNeovascularization, PathologicNitric OxideNitric Oxide Synthase Type IIIProteinsProto-Oncogene Proteins c-aktRGS ProteinsTOR Serine-Threonine KinasesUp-RegulationConceptsHypertrophic responseMiR-182Myocardial hypertrophyEndothelial-cardiomyocyte crosstalkLV pressure overloadEndothelium-derived NOPlacental growth factorMyocardial hypertrophic responseDevelopment of hypertrophyDegradation of regulatorsMiR-182 targetsHemodynamic demandsPressure overloadPlGF expressionBlood supplyParacrine actionCardiomyocyte hypertrophyMyocardial angiogenesisCardiac angiogenesisTreatment inhibitsHypertrophyAKT/mTORC1 pathwaysNovel targetAkt/Growth factor
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
1991
Myocardial protein turnover in patients with coronary artery disease. Effect of branched chain amino acid infusion.
Young LH, McNulty PH, Morgan C, Deckelbaum LI, Zaret BL, Barrett EJ. Myocardial protein turnover in patients with coronary artery disease. Effect of branched chain amino acid infusion. Journal Of Clinical Investigation 1991, 87: 554-560. PMID: 1991838, PMCID: PMC296343, DOI: 10.1172/jci115030.Peer-Reviewed Original ResearchConceptsBranched-chain amino acid infusionCoronary artery diseaseAmino acid infusionProtein turnoverBCAA infusionProtein synthesisArtery diseaseAcid infusionAmino acidsMyocardial protein turnoverCardiac double productCoronary blood flowPlasma insulin levelsMyocardial oxygen consumptionHuman heartProtein degradationNegative protein balanceEssential amino acidsMyocardial balanceInsulin levelsDouble productPhenylalanine balanceAnabolic effectsMyocardial uptakePostabsorptive patients
1990
In vivo measurement of myocardial protein turnover using an indicator dilution technique.
Revkin JH, Young LH, Stirewalt WS, Dahl DM, Gelfand RA, Zaret BL, Barrett EJ. In vivo measurement of myocardial protein turnover using an indicator dilution technique. Circulation Research 1990, 67: 902-912. PMID: 2208613, DOI: 10.1161/01.res.67.4.902.Peer-Reviewed Original Research