2020
H19/TET1 axis promotes TGF‐β signaling linked to endothelial‐to‐mesenchymal transition
Cao T, Jiang Y, Li D, Sun X, Zhang Y, Qin L, Tellides G, Taylor HS, Huang Y. H19/TET1 axis promotes TGF‐β signaling linked to endothelial‐to‐mesenchymal transition. The FASEB Journal 2020, 34: 8625-8640. PMID: 32374060, PMCID: PMC7364839, DOI: 10.1096/fj.202000073rrrrr.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCells, CulturedCoronary VesselsEpithelial-Mesenchymal TransitionHuman Umbilical Vein Endothelial CellsHumansMiceMice, Inbred C57BLMice, KnockoutMixed Function OxygenasesProto-Oncogene ProteinsRNA Processing, Post-TranscriptionalRNA, Long NoncodingSignal TransductionTransforming Growth Factor betaConceptsTGF-β signalingCardiovascular diseaseHuman umbilical vein endothelial cellsEndothelial cellsEndothelial activationMesenchymal transitionMouse pulmonary microvascular endothelial cellsPulmonary microvascular endothelial cellsHuman atherosclerotic coronary arteriesAtherosclerotic coronary arteriesMicrovascular endothelial cellsPrimary human umbilical vein endothelial cellsUmbilical vein endothelial cellsAortic endothelial cellsEndothelial dysfunctionVein endothelial cellsCoronary arteryRisk factorsHyperglycemic conditionsH19 expressionAberrant expressionEndMTH19 lncRNATET1 expressionMolecular underpinnings
2011
Wild-type LRP6 inhibits, whereas atherosclerosis-linked LRP6R611C increases PDGF-dependent vascular smooth muscle cell proliferation
Keramati AR, Singh R, Lin A, Faramarzi S, Ye ZJ, Mane S, Tellides G, Lifton RP, Mani A. Wild-type LRP6 inhibits, whereas atherosclerosis-linked LRP6R611C increases PDGF-dependent vascular smooth muscle cell proliferation. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 1914-1918. PMID: 21245321, PMCID: PMC3033290, DOI: 10.1073/pnas.1019443108.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cell proliferationSmooth muscle cell proliferationLDL receptor-related protein 6Muscle cell proliferationEarly atherosclerosisHuman atherosclerotic coronary arteriesCell proliferationAtherosclerotic coronary arteriesPDGF receptor βPDGF-dependent regulationCoronary arterySmooth muscleVSMC proliferationReceptor βSMC proliferationCell cycle activityAtherosclerosisKey mediatorCritical modulatorProtein 6PDGF SignalingDifferential effectsProliferationFurther investigationCell cycle
2009
Interleukin-17 and Interferon-γ Are Produced Concomitantly by Human Coronary Artery–Infiltrating T Cells and Act Synergistically on Vascular Smooth Muscle Cells
Eid RE, Rao DA, Zhou J, Lo SF, Ranjbaran H, Gallo A, Sokol SI, Pfau S, Pober JS, Tellides G. Interleukin-17 and Interferon-γ Are Produced Concomitantly by Human Coronary Artery–Infiltrating T Cells and Act Synergistically on Vascular Smooth Muscle Cells. Circulation 2009, 119: 1424-1432. PMID: 19255340, PMCID: PMC2898514, DOI: 10.1161/circulationaha.108.827618.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedCD4-Positive T-LymphocytesCells, CulturedChemokine CXCL10Coronary Artery DiseaseCoronary VesselsFemaleGene Expression RegulationHumansInflammation MediatorsInterferon-gammaInterleukin-17Interleukin-6Interleukin-8InterleukinsMaleMiddle AgedMuscle, Smooth, VascularMyocytes, Smooth MuscleReceptors, InterferonReceptors, Interleukin-17Signal TransductionT-Lymphocyte SubsetsTransforming Growth Factor beta1VasculitisConceptsVascular smooth muscle cellsSmooth muscle cellsIL-17IFN-gammaT cellsCoronary atherosclerosisMuscle cellsCoronary arteryIL-6Signature cytokinesIL-17 plasma levelsCultured vascular smooth muscle cellsIL-17 synthesisIL-17 responsesHuman coronary atherosclerosisIL-17 secretionSubset of patientsIL-17 producersT helper cellsIFN-gamma synthesisIFN-gamma producersYoung healthy individualsAtherosclerotic coronary arteriesHuman coronary arteriesTh17 cells
2007
An Inflammatory Pathway of IFN-γ Production in Coronary Atherosclerosis
Ranjbaran H, Sokol SI, Gallo A, Eid RE, Iakimov AO, D’Alessio A, Kapoor JR, Akhtar S, Howes CJ, Aslan M, Pfau S, Pober JS, Tellides G. An Inflammatory Pathway of IFN-γ Production in Coronary Atherosclerosis. The Journal Of Immunology 2007, 178: 592-604. PMID: 17182600, DOI: 10.4049/jimmunol.178.1.592.Peer-Reviewed Original ResearchConceptsIL-12/ILIFN-gamma-inducible chemokinesCoronary atherosclerosisIL-12IL-18IFN-gammaPlasma levelsT cellsTh1-type cytokine productionHuman atherosclerotic coronary arteriesAcute coronary syndromeSubset of patientsHuman coronary atherosclerosisTh1-type cytokinesC-reactive proteinIFN-γ productionElevated plasma levelsPlasma of patientsInnate immune responseAtherosclerotic coronary arteriesCoronary syndromeSystemic inflammationCardiac catheterizationCardiopulmonary bypassGamma secretion
2006
Heparin Displaces Interferon-γ–Inducible Chemokines (IP-10, I-TAC, and Mig) Sequestered in the Vasculature and Inhibits the Transendothelial Migration and Arterial Recruitment of T Cells
Ranjbaran H, Wang Y, Manes TD, Yakimov AO, Akhtar S, Kluger MS, Pober JS, Tellides G. Heparin Displaces Interferon-γ–Inducible Chemokines (IP-10, I-TAC, and Mig) Sequestered in the Vasculature and Inhibits the Transendothelial Migration and Arterial Recruitment of T Cells. Circulation 2006, 114: 1293-1300. PMID: 16940188, DOI: 10.1161/circulationaha.106.631457.Peer-Reviewed Original ResearchMeSH KeywordsAnti-Inflammatory AgentsCell MovementCells, CulturedChemokine CXCL10Chemokine CXCL11Chemokine CXCL9ChemokinesChemokines, CXCCoronary Artery DiseaseCoronary VesselsEndothelium, VascularHeparinHeparin AntagonistsHumansInterferon-gammaInterleukin-12ProtaminesProtein BindingReceptors, ChemokineReceptors, CXCR3T-LymphocytesTh1 CellsConceptsIP-10Heparin administrationCoronary arteryEndothelial cellsI-TACT cellsIFN-gamma-dependent productionTh1-type inflammatory diseasesI-TAC/CXCL11IP-10/CXCL10IFN-gamma-producing Th1 cellsTransendothelial migrationInflammatory arterial diseaseNonanticoagulant heparin derivativesCoronary artery bypassChemokines IP-10/CXCL10Memory T cellsT helper cellsMIG/CXCL9IFN-gamma responsesEffect of heparinAtherosclerotic coronary arteriesHuman coronary arteriesImmunodeficient mouse hostsCultured endothelial cells
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