Raja Chakraborty, PhD
Associate Research Scientist (Cardiovascular Medicine)DownloadHi-Res Photo
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Cardiovascular Medicine
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Associate Research Scientist (Cardiovascular Medicine)
Appointments
Cardiovascular Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- PhD
- University of Manitoba, Biochemistry/Pharmacology (2014)
- MS
- Australian National University, Biotechnology (2008)
- BE
- Institute of Technology and Marine Engineering, Biotechnology (2006)
Research
Research at a Glance
Yale Co-Authors
Frequent collaborators of Raja Chakraborty's published research.
Publications Timeline
A big-picture view of Raja Chakraborty's research output by year.
Daniel Greif, MD
Kathleen Martin, PhD
John Hwa, MD, PhD, FRACP
Payel Chatterjee, PhD
Patrick Gallagher, MD, BS
Carlos Fernandez-Hernando, PhD
24Publications
1,717Citations
Publications
Featured Publications
Histone Acetyltransferases p300 and CBP Coordinate Distinct Chromatin Remodeling Programs in Vascular Smooth Muscle Plasticity
Chakraborty R, Ostriker AC, Xie Y, Dave JM, Gamez-Mendez A, Chatterjee P, Abu Y, Valentine J, Lezon-Geyda K, Greif DM, Schulz VP, Gallagher PG, Sessa WC, Hwa J, Martin KA. Histone Acetyltransferases p300 and CBP Coordinate Distinct Chromatin Remodeling Programs in Vascular Smooth Muscle Plasticity. Circulation 2022, 145: 1720-1737. PMID: 35502657, DOI: 10.1161/circulationaha.121.057599.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHistone acetylationContractile genesContractile protein expressionPhenotypic switchingHistone acetyl transferase p300Human intimal hyperplasiaPlatelet-derived growth factor treatmentAcetyl transferase p300Key regulatory mechanismSmooth muscle cell phenotypeP300 expressionP300-dependent acetylationSmooth muscle plasticityDistinct functional interactionsMuscle cell phenotypeProtein expressionIntimal hyperplasiaRole of p300Methylcytosine dioxygenase TET2Chromatin modificationsEpigenetic regulationVSMC phenotypic switchingSpecific histoneCardiovascular diseaseMaster regulatorJAGGED1/NOTCH3 activation promotes aortic hypermuscularization and stenosis in elastin deficiency
Dave JM, Chakraborty R, Ntokou A, Saito J, Saddouk FZ, Feng Z, Misra A, Tellides G, Riemer RK, Urban Z, Kinnear C, Ellis J, Mital S, Mecham R, Martin KA, Greif DM. JAGGED1/NOTCH3 activation promotes aortic hypermuscularization and stenosis in elastin deficiency. Journal Of Clinical Investigation 2022, 132: e142338. PMID: 34990407, PMCID: PMC8884911, DOI: 10.1172/jci142338.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSmooth muscle cellsSupravalvular aortic stenosisEndothelial cellsElastin insufficiencyObstructive arterial diseaseAortic smooth muscle cellsΓ-secretaseAortic vascular cellsPotential therapeutic targetNotch3 intracellular domainNotch ligand Jagged1Aortic stenosisArterial diseasePathological featuresPharmacological treatmentJag1 deletionLuminal obstructionMouse modelNotch3 activationTherapeutic targetSMC accumulationPathway upregulationAortic samplesMice displayNotch3 deletionTET2 Protects Against Vascular Smooth Muscle Cell Apoptosis and Intimal Thickening in Transplant Vasculopathy
Ostriker AC, Xie Y, Chakraborty R, Sizer AJ, Bai Y, Ding M, Song WL, Huttner A, Hwa J, Martin KA. TET2 Protects Against Vascular Smooth Muscle Cell Apoptosis and Intimal Thickening in Transplant Vasculopathy. Circulation 2021, 144: 455-470. PMID: 34111946, PMCID: PMC8643133, DOI: 10.1161/circulationaha.120.050553.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAllograftsAnimalsApoptosisBiomarkersDioxygenasesDisease Models, AnimalDisease SusceptibilityDNA-Binding ProteinsHeart TransplantationHumansImmunohistochemistryInterferon-gammaMiceMice, KnockoutMyocytes, Smooth MuscleSignal TransductionSTAT1 Transcription FactorTunica IntimaVascular DiseasesConceptsCoronary allograft vasculopathyGraft arteriopathyIntimal thickeningCAV progressionRole of TET2VSMC apoptosisTransplant samplesGraft modelHigh-dose ascorbic acidTET2 expressionVSMC phenotypeContext of transplantCoronary blood flowEffect of IFNγTET2 activityTET2 depletionSmooth muscle cell apoptosisVascular smooth muscle cell apoptosisMuscle cell apoptosisAllograft vasculopathyDevastating sequelaeMedial thinningAortic graftHeart transplantTransplant failureTargeting smooth muscle cell phenotypic switching in vascular disease
Chakraborty R, Chatterjee P, Dave JM, Ostriker AC, Greif DM, Rzucidlo EM, Martin KA. Targeting smooth muscle cell phenotypic switching in vascular disease. JVS Vascular Science 2021, 2: 79-94. PMID: 34617061, PMCID: PMC8489222, DOI: 10.1016/j.jvssci.2021.04.001.Peer-Reviewed Original ResearchCitationsAltmetricConceptsSingle-cell transcriptomicsVascular smooth muscle cellsVSMC phenotypic modulationPhenotypic plasticityCell transcriptomicsPhenotypic modulationMature vascular smooth muscle cellsSmooth muscle cell phenotypicLineage tracing methodStriking diversityFundamental new insightsMolecular mechanismsFate mappingRemarkable plasticityBromodomain inhibitorsHistone deacetylasePhenotypic switchingPharmacologic inhibitorsGenetic targetingVSMC phenotypicDruggable pathwaysSmooth muscle cellsOligoclonal lesionsTranscriptomicsRecent discovery
2024
Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis
Joshi D, Coon B, Chakraborty R, Deng H, Yang Z, Babar M, Fernandez-Tussy P, Meredith E, Attanasio J, Joshi N, Traylor J, Orr A, Fernandez-Hernando C, Libreros S, Schwartz M. Endothelial γ-protocadherins inhibit KLF2 and KLF4 to promote atherosclerosis. Nature Cardiovascular Research 2024, 3: 1035-1048. PMID: 39232138, PMCID: PMC11399086, DOI: 10.1038/s44161-024-00522-z.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsAtherosclerosisCadherin Related ProteinsCadherinsDisease Models, AnimalEndothelial CellsHuman Umbilical Vein Endothelial CellsHumansKruppel-Like Factor 4Kruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLMice, KnockoutPlaque, AtheroscleroticReceptors, NotchSignal TransductionConceptsAtherosclerotic cardiovascular diseaseIntracellular domainNotch intracellular domainTranscription factor KLF2Mechanisms of vascular inflammationAnti-inflammatory programVascular endothelial cellsHost defenseCleavage resultsAntibody blockadeGenetic deletionVascular inflammationViral infectionImmune systemEndothelial cellsCardiovascular diseasePromote atherosclerosisBlood flowKLF2KLF4Suppressive signalsEndotheliumMechanistic studiesLoss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis
Dave J, Chakraborty R, Agyemang A, Ntokou A, Saito J, Ballabh P, Martin K, Greif D. Loss of TGFβ-Mediated Repression of Angiopoietin-2 in Pericytes Underlies Germinal Matrix Hemorrhage Pathogenesis. Stroke 2024, 55: 2340-2352. PMID: 39129597, PMCID: PMC11347087, DOI: 10.1161/strokeaha.123.045248.Peer-Reviewed Original ResearchAltmetricConceptsAngiopoietin-2Germinal matrix hemorrhage-intraventricular hemorrhagePerinatal lethalityEndothelial cell hyperproliferationEndothelial cellsBrain pericytesGenetic inhibitionVascular cellsBlood-brain barrier integrityBlood-brain barrier developmentBrain vascular cellsAbnormal vessel morphologyVessel morphologyProlonged survivalRegulating cross-talkMutant endothelial cellsHuman brain pericytesGerminal matrixCell hyperproliferationPhosphorylates Tie2Embryonic miceCellular sourceBarrier integrityGenetic ablationTherapeutic effectAbstract 2121: SUV39H1 Mediated Regulation Of KLF4 And KDM4a Coordinate Smooth Muscle Cell Phenotypic Plasticity
Chatterjee P, Chakraborty R, Sizer A, Xie Y, Hwa J, Martin K. Abstract 2121: SUV39H1 Mediated Regulation Of KLF4 And KDM4a Coordinate Smooth Muscle Cell Phenotypic Plasticity. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: a2121-a2121. DOI: 10.1161/atvb.44.suppl_1.2121.Peer-Reviewed Original ResearchConceptsRNA-seqPhenotypic plasticityEpigenetic regulationH3K9me3 repressive marksRNA-seq transcriptomicsContractile genesEpigenetic transcriptional repressionCell phenotypic plasticityH3K9me3 markExpression of SUV39H1Repressive marksTranscriptional repressionChromatin immunoprecipitationHistone methyltransferaseDedifferentiation in vitroIn vivoSUV39H1 knockdownH3K9me3MRNA stabilitySUV39H1Gene expressionPlasticity of vascular smooth muscle cellsRegulation of Klf4GenesH3K9me3 expressionAbstract 1147: Crosstalk Between Alk5 And Mtorc1 Signaling Promotes VSMC Differentiation And The Therapeutic Effect Of Rapamycin
Chakraborty R, Chatterjee P, Dave J, Obrien B, Joshi D, Schulz V, Greif D, Hwa J, Gallagher P, Martin K. Abstract 1147: Crosstalk Between Alk5 And Mtorc1 Signaling Promotes VSMC Differentiation And The Therapeutic Effect Of Rapamycin. Arteriosclerosis Thrombosis And Vascular Biology 2024, 44: a1147-a1147. DOI: 10.1161/atvb.44.suppl_1.1147.Peer-Reviewed Original ResearchConceptsVascular smooth muscle cellsTherapeutic effect of rapamycinEffects of rapamycinVSMC differentiationContractile genesConsistent with in vitro findingsRapamycin treatmentCarotid artery injuryHuman coronary artery SMCsVascular smooth muscle cell differentiationIntimal hyperplasiaSmooth muscle cellsCoronary artery SMCsMTORC1 inhibitor rapamycinPhosphorylation of Smad2/3Inhibition of ALK5Smad-binding elementSmad transcription factorsALK5 activityArterial injuryArtery SMCsKnockout miceInhibition of mTORC1Vascular smooth muscle cell plasticityMuscle cells
2023
Multimodality Platelet Evaluation By Mass Cytometry and Genetic Analysis in Patients with Bleeding Disorders
Gu S, Gallagher P, Butt A, Gu V, Lezon-Geyda K, Schulz V, Prozora S, Lee A, Neparidze N, Bar N, Martin K, Cornell J, Chirico G, Chakraborty R, Rinder H, Hwa J, Bona R. Multimodality Platelet Evaluation By Mass Cytometry and Genetic Analysis in Patients with Bleeding Disorders. Blood 2023, 142: 1197. DOI: 10.1182/blood-2023-177946.Peer-Reviewed Original ResearchConceptsBleeding tendencyBleeding disorderPlatelet markersPlatelet aggregometryMass cytometryPlatelet functionPlatelet disordersSingle-center prospective studyLow-risk groupAbnormal bleeding tendencyQualitative platelet disordersLarge patient cohortQuantitative platelet disordersCommon underlying causeGenetic variantsMultimodality evaluationTotal patientsRisk stratificationLaboratory suspicionPlatelet dysfunctionProspective studyPatient cohortUnivariate analysisPlatelet volumeRisk groupsThe age of bone marrow dictates the clonality of smooth muscle-derived cells in atherosclerotic plaques
Kabir I, Zhang X, Dave J, Chakraborty R, Qu R, Chandran R, Ntokou A, Gallardo-Vara E, Aryal B, Rotllan N, Garcia-Milian R, Hwa J, Kluger Y, Martin K, Fernández-Hernando C, Greif D. The age of bone marrow dictates the clonality of smooth muscle-derived cells in atherosclerotic plaques. Nature Aging 2023, 3: 64-81. PMID: 36743663, PMCID: PMC9894379, DOI: 10.1038/s43587-022-00342-5.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsAtherosclerotic plaquesBone marrowSmooth muscle-derived cellsSMC progenitorsAtherosclerotic plaque cellsSmooth muscle cell progenitorsPredominant risk factorCause of deathNovel therapeutic strategiesTNF receptor 1Muscle-derived cellsAged bone marrowAged BMEffect of agePlaque burdenAged miceRisk factorsTumor necrosisTherapeutic strategiesPlaque cellsMyeloid cellsReceptor 1Integrin β3Cell progenitorsAtherosclerosis
News
News
- January 29, 2023
Yale Study Finds Aging of Bone Marrow Accelerates Atherosclerotic Plaque Formation
- February 15, 2022Source: Yale Daily News
Yale study identifies potential target genes to develop therapeutic treatments for heart defect
- February 07, 2022
Potential Therapeutic Target for Aortic Stenosis Identified