2024
Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy
Liu X, Li B, Wang S, Zhang E, Schultz M, Touma M, Da Rocha A, Evans S, Eichmann A, Herron T, Chen R, Xiong D, Jaworski A, Weiss S, Si M. Stromal Cell-SLIT3/Cardiomyocyte-ROBO1 Axis Regulates Pressure Overload-Induced Cardiac Hypertrophy. Circulation Research 2024, 134: 913-930. PMID: 38414132, PMCID: PMC10977056, DOI: 10.1161/circresaha.122.321292.Peer-Reviewed Original ResearchConceptsTransverse aortic constrictionAortic constrictionPressure overloadCardiomyocyte hypertrophyVascular mural cellsCardiomyocyte hypertrophy in vitroDecreased left ventricular hypertrophyStimulate cardiomyocyte hypertrophyCongenital heart defectsCell-specific knockoutLeft ventricular functionAdverse cardiac remodelingVentricular pressure overloadCardiomyocyte-specific deletionMural cellsHypertrophy in vitroPressure overload stressCardiac stromal cellsMyocardial tissue samplesEffects in vitroIn vitro studiesHypertrophy-related genesHeart defectsRegulate cardiac developmentVentricular function
2022
Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas
Zhang H, Li B, Huang Q, López-Giráldez F, Tanaka Y, Lin Q, Mehta S, Wang G, Graham M, Liu X, Park I, Eichmann A, Min W, Zhou J. Mitochondrial dysfunction induces ALK5-SMAD2-mediated hypovascularization and arteriovenous malformations in mouse retinas. Nature Communications 2022, 13: 7637. PMID: 36496409, PMCID: PMC9741628, DOI: 10.1038/s41467-022-35262-w.Peer-Reviewed Original ResearchConceptsMitochondrial dysfunctionThioredoxin 2Single-cell RNA-seq analysisRNA-seq analysisMutant miceNuclear genesMitochondrial proteinsMitochondrial localizationHuman retinal diseasesTranscriptional factorsGene expressionMutant retinasMitochondrial activityExtracellular matrixNovel mechanismVascular maturationArteriovenous malformationsGenetic deficiencyVessel growthSmad2Mouse retinaVascular malformationsMechanistic studiesBasement membraneRetinal vascular malformations
2007
The Notch ligand Delta-like 4 negatively regulates endothelial tip cell formation and vessel branching
Suchting S, Freitas C, le Noble F, Benedito R, Bréant C, Duarte A, Eichmann A. The Notch ligand Delta-like 4 negatively regulates endothelial tip cell formation and vessel branching. Proceedings Of The National Academy Of Sciences Of The United States Of America 2007, 104: 3225-3230. PMID: 17296941, PMCID: PMC1805603, DOI: 10.1073/pnas.0611177104.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAmyloid Precursor Protein SecretasesAnimalsCalcium-Binding ProteinsEndothelium, VascularGamma-Aminobutyric AcidImmunohistochemistryIn Situ HybridizationIntracellular Signaling Peptides and ProteinsMembrane ProteinsMiceMice, Mutant StrainsReceptors, Vascular Endothelial Growth FactorRetinal VesselsSignal TransductionTriglyceridesVascular Endothelial Growth Factor AConceptsTip cell formationEndothelial tip cell formationTip cellsNotch ligand DeltaCell formationCell marker genesEndothelial tip cellsVessel branchingLigand DeltaExpression of Dll4Vascular network formationTransmembrane ligandsNotch receptorsMarker genesNegative regulatorAngiogenic sproutingVEGF receptor 2VEGF stimulationFilopodia extensionGamma-secretase inhibitorsGrowth factor VEGFVascular sproutingPharmacological inhibitionDll4Heterozygous deletion
2004
Retinoic acid controls blood vessel formation by modulating endothelial and mural cell interaction via suppression of Tie2 signaling in vascular progenitor cells
Suzuki Y, Komi Y, Ashino H, Yamashita J, Inoue J, Yoshiki A, Eichmann A, Amanuma H, Kojima S. Retinoic acid controls blood vessel formation by modulating endothelial and mural cell interaction via suppression of Tie2 signaling in vascular progenitor cells. Blood 2004, 104: 166-169. PMID: 15026310, DOI: 10.1182/blood-2003-09-3293.Peer-Reviewed Original ResearchConceptsVascular progenitor cellsAll-trans retinoic acidChicken chorioallantoic membraneEndothelial cellsTie2 signalingProgenitor cellsBlood vessel formationMural cellsEpithelial layerExpression of angiopoietin-2Vessel formationRetinoic acidImpaired vascular remodelingImpaired branchingAngiopoietin-2Ang-1Vascular remodelingRo41-5253Cell interactionsMural cell interactions