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
2012
Vascular adaptation to a dysfunctional endothelium as a consequence of Shb deficiency
Christoffersson G, Zang G, Zhuang ZW, Vågesjö E, Simons M, Phillipson M, Welsh M. Vascular adaptation to a dysfunctional endothelium as a consequence of Shb deficiency. Angiogenesis 2012, 15: 469-480. PMID: 22562363, PMCID: PMC4059510, DOI: 10.1007/s10456-012-9275-z.Peer-Reviewed Original ResearchConceptsShb knockout mouseWild-type situationShb adapter proteinPatho-physiological responsesKnockout miceAdapter proteinAdherens junctionsShb deficiencyFunction of VEGFVE-cadherinVivo angiogenesisPhysiological conditionsAltered propertiesReceptor VEGFR-2Growth factorVascular endothelial growth factorVEGFR-2
2010
Aging‐induced collateral impairment: role of arterial rarefaction, decreased eNOS expression/signaling, and increased susceptibility of endothelial cells to apoptosis
Epstein S, Wang J, Peng X, Zhuang Z, Simons M, Xue Z, Burnett M. Aging‐induced collateral impairment: role of arterial rarefaction, decreased eNOS expression/signaling, and increased susceptibility of endothelial cells to apoptosis. The FASEB Journal 2010, 24: 294.3-294.3. DOI: 10.1096/fasebj.24.1_supplement.294.3.Peer-Reviewed Original ResearchWild-type miceEndothelial cellsOld miceEndothelial nitric oxide synthase proteinNitric oxide synthase proteinOld wild-type micePositive animal studiesYoung wild-type miceENOS-KO miceENOS knockout miceDisappointing clinical resultsPre-existing arteriolesVessel phenotypeENOS expressionENOS proteinKO miceC57 miceClinical resultsYoung miceArteriolar rarefactionAge-induced changesKnockout miceAnimal studiesTherapeutic interventionsAngiogenesis therapy