2024
Endothelial TGF-β Signaling Regulates Endothelial-Mesenchymal Transition During Arteriovenous Fistula Remodeling in Mice With Chronic Kidney Disease
Zhang W, Gonzalez L, Li X, Bai H, Li Z, Taniguchi R, Langford J, Ohashi Y, Thaxton C, Aoyagi Y, Yatsula B, Martin K, Goodwin J, Tellides G, Long X, Shu C, Dardik A. Endothelial TGF-β Signaling Regulates Endothelial-Mesenchymal Transition During Arteriovenous Fistula Remodeling in Mice With Chronic Kidney Disease. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 2509-2526. PMID: 39297205, PMCID: PMC11593991, DOI: 10.1161/atvbaha.124.320933.Peer-Reviewed Original ResearchChronic kidney diseaseTGF-b signalingArteriovenous fistula patencyArteriovenous fistulaKidney diseaseAVF patencyEndothelial cellsAssociated with endothelial injuryArteriovenous fistula diameterImprove AVF patencyIncreased outward remodelingReduced patencyInduced endothelial-to-mesenchymal transitionAortocaval fistula modelSmooth muscle cell proliferationArteriovenous fistula failureAttenuated EndMTEnd-stage kidney diseaseHuman arteriovenous fistulaeSmooth muscle cellsMuscle cell proliferationEndothelial-to-mesenchymal transitionMouse endothelial cellsInhibition of EndMTEndothelial-mesenchymal transitionDe Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report
Ellis M, Riaz M, Huang Y, Anderson C, Hoareau M, Li X, Luo H, Lee S, Park J, Luo J, Batty L, Huang Q, Lopez C, Reinhardt D, Tellides G, Qyang Y. De Novo Elastin Assembly Alleviates Development of Supravalvular Aortic Stenosis—Brief Report. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: 1674-1682. PMID: 38752350, PMCID: PMC11209776, DOI: 10.1161/atvbaha.124.320790.Peer-Reviewed Original ResearchSupravalvular aortic stenosisVascular smooth muscle cellsSmooth muscle cellsMuscle cellsAortic stenosisMedial vascular smooth muscle cellsVascular proliferative diseasesEpigallocatechin gallate treatmentProliferative abnormalitiesPreclinical findingsHeart failureLuminal occlusionMouse modelCell hyperproliferationDefective elastinProliferative diseasesCardiovascular disordersFormation of elastinTherapeutic interventionsElastin assemblyElastin depositionStenosisMiceAortic mechanicsImproper formationMultiscale computational model of aortic remodeling following postnatal disruption of TGFβ signaling
Estrada A, Irons L, Tellides G, Humphrey J. Multiscale computational model of aortic remodeling following postnatal disruption of TGFβ signaling. Journal Of Biomechanics 2024, 169: 112152. PMID: 38763809, PMCID: PMC11141772, DOI: 10.1016/j.jbiomech.2024.112152.Peer-Reviewed Original ResearchAdult aortaTGFB signalingSmooth muscle cellsAortic remodelingCardiac-inducedMouse modelNormal mechanical loadingMuscle cellsPostnatal developmentHemodynamic loadNormal loadAortaMechanical homeostasisMechanical loadingMultiscale computational modelIncreasing loadLoadCell signalingGene productsStructural integrityIntimomedial tears of the aorta heal by smooth muscle cell-mediated fibrosis without atherosclerosis
Hassab A, Hur D, Vallabhajosyula P, Tellides G, Assi R. Intimomedial tears of the aorta heal by smooth muscle cell-mediated fibrosis without atherosclerosis. JCI Insight 2024, 9: e172437. PMID: 38592807, PMCID: PMC11141924, DOI: 10.1172/jci.insight.172437.Peer-Reviewed Original ResearchConceptsDepartment of SurgerySmooth muscle cellsCellular response to injuryResponse to injuryImmunofluorescence confocal microscopyVessel wall repairPrimary lesionAscending aortaConduit functionAneurysmal diseaseDense fibrosisRadiological signsMural hematomaTear progressionMuscle cellsNon-hemorrhagicErythrocyte extravasationWall repairAortaTear completionInduce atherosclerosisHealed lesionsScattered leukocytesMinimal injuryConclusionThese findings
2023
Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria
Murtada S, Kawamura Y, Cavinato C, Wang M, Ramachandra A, Spronck B, Li D, Tellides G, Humphrey J. Biomechanical and transcriptional evidence that smooth muscle cell death drives an osteochondrogenic phenotype and severe proximal vascular disease in progeria. Biomechanics And Modeling In Mechanobiology 2023, 22: 1333-1347. PMID: 37149823, PMCID: PMC10544720, DOI: 10.1007/s10237-023-01722-5.Peer-Reviewed Original ResearchConceptsPulse wave velocitySmooth muscle cell deathMuscle cell deathDisease processOsteochondrogenic phenotypeAdverse extracellular matrix remodelingImportant cardiovascular implicationsProgressive aortic diseaseProximal elastic arteriesVentricular diastolic dysfunctionProgressive disease processSmooth muscle cellsCell deathCardiovascular sequelaeDiastolic dysfunctionCardiovascular implicationsExtracellular matrix remodelingAortic diseasePrimary diagnosisVascular diseaseAccumulation of proteoglycansMuscular arteriesAortic structureAortic wallLate calcificationFN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome
Chen M, Cavinato C, Hansen J, Tanaka K, Ren P, Hassab A, Li D, Youshao E, Tellides G, Iyengar R, Humphrey J, Schwartz M. FN (Fibronectin)-Integrin α5 Signaling Promotes Thoracic Aortic Aneurysm in a Mouse Model of Marfan Syndrome. Arteriosclerosis Thrombosis And Vascular Biology 2023, 43: e132-e150. PMID: 36994727, PMCID: PMC10133209, DOI: 10.1161/atvbaha.123.319120.Peer-Reviewed Original ResearchConceptsContractile gene expressionSmooth muscle cellsGene expressionMgR miceWild-type smooth muscle cellsMarfan miceAortic aneurysmMouse modelMarfan syndromeMouse aortic smooth muscle cellsPathogenesis of TAACytoplasmic domainVascular smooth muscle cellsThoracic aortic aneurysmAortic smooth muscle cellsCultured smooth muscle cellsNF-kB activationNF-kB inhibitionMolecular mechanismsIntegrin α2ECM remodelingElastic fiber integrityPhenotypic modulationMarfan's aneurysmsMgR/
2021
Adventitial remodeling protects against aortic rupture following late smooth muscle-specific disruption of TGFβ signaling
Kawamura Y, Murtada S, Gao F, Liu X, Tellides G, Humphrey J. Adventitial remodeling protects against aortic rupture following late smooth muscle-specific disruption of TGFβ signaling. Journal Of The Mechanical Behavior Of Biomedical Materials 2021, 116: 104264. PMID: 33508556, PMCID: PMC7959590, DOI: 10.1016/j.jmbbm.2020.104264.Peer-Reviewed Original ResearchConceptsAortic dissectionMouse modelAortic wallCompensatory changesThoracic aortic dissectionMuscle-specific disruptionSmooth muscle cellsLoss of TGFβMedial integrityAortic ruptureClinical presentationMuscle cellsQuantitative histologyMatrix turnoverTGFβ receptorsDissectionWall stressTGFβType IIndividual subjectsSpecific disruptionVivo valuesExaminationRupture
2000
Interferon-γ elicits arteriosclerosis in the absence of leukocytes
Tellides G, Tereb D, Kirkiles-Smith N, Kim R, Wilson J, Schechner J, Lorber M, Pober J. Interferon-γ elicits arteriosclerosis in the absence of leukocytes. Nature 2000, 403: 207-211. PMID: 10646607, DOI: 10.1038/35003221.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsArteriosclerosisCell DivisionCells, CulturedCoronary VesselsHistocompatibility AntigensHumansImage Processing, Computer-AssistedImmunohistochemistryInterferon-gammaLeukocytesMiceMice, SCIDMuscle, Smooth, VascularPlatelet-Derived Growth FactorReceptor, Platelet-Derived Growth Factor betaSwineTransplantation, HeterologousConceptsVascular smooth muscle cellsGraft arteriosclerosisIntimal expansionAbsence of leukocytesLesions of atherosclerosisSmooth muscle cellsAllogeneic transplantationArteriosclerotic changesAtheroma formationCytokine interferonExogenous IFNAntigen presentationT cellsImmunodeficient miceMononuclear leukocytesMouse modelArterial intimaIFNMuscle cellsArteriosclerosisLeukocytesHuman arteriesAtherosclerosisCellsTransplantation