2008
Chromogranin B Regulates Calcium Signaling, Nuclear Factor &kgr;B Activity, and Brain Natriuretic Peptide Production in Cardiomyocytes
Heidrich FM, Zhang K, Estrada M, Huang Y, Giordano FJ, Ehrlich BE. Chromogranin B Regulates Calcium Signaling, Nuclear Factor &kgr;B Activity, and Brain Natriuretic Peptide Production in Cardiomyocytes. Circulation Research 2008, 102: 1230-1238. PMID: 18420944, PMCID: PMC2952358, DOI: 10.1161/circresaha.107.166033.Peer-Reviewed Original ResearchMeSH KeywordsAge FactorsAngiotensin IIAnimalsCalciumCalcium SignalingCardiomegalyCells, CulturedChromogranin BInositol 1,4,5-Trisphosphate ReceptorsMyocytes, CardiacNatriuretic Peptide, BrainNFATC Transcription FactorsNF-kappa BPromoter Regions, GeneticRatsTranscription, GeneticVasoconstrictor AgentsConceptsBrain natriuretic peptideAngiotensin IICardiac hypertrophyBNP productionChromogranin BNuclear factorNuclear factor-kappaB activityNatriuretic peptide productionActivated T cellsNuclear factor-kappaBLuciferase reporter assaysHeart failureNatriuretic peptideBasal secretionCardiovascular diseaseT cellsKappaB activityFactor-kappaBHypertrophyCGB expressionBNP promoterPotent inducerAdult cardiomyocytesOctapeptide hormoneCalcium signaling
2007
Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions
Zhang H, Luo Y, Zhang W, He Y, Dai S, Zhang R, Huang Y, Bernatchez P, Giordano FJ, Shadel G, Sessa WC, Min W. Endothelial-Specific Expression of Mitochondrial Thioredoxin Improves Endothelial Cell Function and Reduces Atherosclerotic Lesions. American Journal Of Pathology 2007, 170: 1108-1120. PMID: 17322393, PMCID: PMC1864879, DOI: 10.2353/ajpath.2007.060960.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAortaApolipoproteins EAtherosclerosisCells, CulturedEndothelial CellsFlow CytometryImmunoblottingImmunohistochemistryMiceMice, TransgenicMicroscopy, ConfocalMitochondrial ProteinsNitric OxideReactive Oxygen SpeciesReverse Transcriptase Polymerase Chain ReactionThioredoxinsVasodilationConceptsTg miceAtherosclerotic lesionsOxidative stressNitric oxide levelsEC functionDeficient mouse modelEndothelial cell functionAtherosclerosis developmentEnhanced vasodilationVascular EC functionEndothelium functionApolipoprotein EControl littermatesMouse modelOxide levelsMice showCapacity of ECEndothelial-specific expressionEndothelial cellsCritical roleReactive oxygen speciesCell functionMiceTotal antioxidantsLesions
2004
Loss of HIF-1α in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis
Tang N, Wang L, Esko J, Giordano FJ, Huang Y, Gerber HP, Ferrara N, Johnson RS. Loss of HIF-1α in endothelial cells disrupts a hypoxia-driven VEGF autocrine loop necessary for tumorigenesis. Cancer Cell 2004, 6: 485-495. PMID: 15542432, DOI: 10.1016/j.ccr.2004.09.026.Peer-Reviewed Original ResearchAnimalsCell HypoxiaCell ProliferationCells, CulturedChemotaxisEndothelial CellsGene Expression RegulationHypoxia-Inducible Factor 1, alpha SubunitMiceNeoplasmsNeovascularization, PathologicTranscription FactorsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-2Wound Healing
2002
Corticotropin-releasing factor receptor 2 is a tonic suppressor of vascularization
Bale TL, Giordano FJ, Hickey RP, Huang Y, Nath AK, Peterson KL, Vale WW, Lee KF. Corticotropin-releasing factor receptor 2 is a tonic suppressor of vascularization. Proceedings Of The National Academy Of Sciences Of The United States Of America 2002, 99: 7734-7739. PMID: 12032352, PMCID: PMC124337, DOI: 10.1073/pnas.102187099.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsCapillariesCell DivisionCells, CulturedEndothelial Growth FactorsEndothelium, VascularGene Expression RegulationLymphokinesMiceMice, KnockoutMuscle, Smooth, VascularNeovascularization, PhysiologicReceptors, Corticotropin-Releasing HormoneVascular Endothelial Growth Factor AVascular Endothelial Growth FactorsConceptsCorticotropin-releasing factor receptor 2Smooth muscle cellsCapillary tube formationTube formationCell cycle progressionVascular endothelial growth factorFactor receptor 2Protein phosphorylationRetinoblastoma proteinCycle progressionLigand activationReceptor 2Adult neovascularizationCRFR2-deficient miceCell proliferationIschemic cardiovascular diseasePotential targetAdult vesselsQuiescent stateMuscle cellsEndothelial growth factorGrowth factorSMC proliferationWestern blotCollagen gels