Vinod Ramgolam, PhD
Associate Research Scientist in Medicine (Cardiology)Cards
Contact Info
About
Copy Link
Titles
Associate Research Scientist in Medicine (Cardiology)
Appointments
Cardiovascular Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
Education & Training
- PhD
- National University of Singapore (2001)
- MSc
- Free University (1996)
Research
Copy Link
Research at a Glance
Yale Co-Authors
Frequent collaborators of Vinod Ramgolam's published research.
Publications Timeline
A big-picture view of Vinod Ramgolam's research output by year.
Jeffrey Bender, MD
Nina Stachenfeld, PhD
Timur Yarovinsky, MD, PhD
10Publications
604Citations
Publications
2026
X-inactive specific transcript (XIST) can determine sex differences in cardiovascular drug responses: focus on RNA therapeutics
Yarovinsky T, Ramgolam V, Knezevic I, Stachenfeld N, Bender J. X-inactive specific transcript (XIST) can determine sex differences in cardiovascular drug responses: focus on RNA therapeutics. Frontiers In Pharmacology 2026, 16: 1716863. PMID: 41601966, PMCID: PMC12832541, DOI: 10.3389/fphar.2025.1716863.Peer-Reviewed Original ResearchAltmetricConceptsCardiovascular drug responsePost-transcriptional regulationTranscriptional repressionX chromosomeTranscriptional repression of genesX-inactive specific transcriptRegulation of gene expressionRNA therapeuticsDrug responseInactive X chromosomePost-transcriptional regulation of gene expressionRNA-binding proteinsRepression of genesRandom X-chromosome inactivationX-chromosome inactivationX-linked recessive disorderFemale genomesGene dosageEpigenetic mechanismsBinding proteinGene expressionSpecific transcriptDrug development targetMiRNA spongesRNA
2011
B Cells as a Therapeutic Target for IFN-β in Relapsing–Remitting Multiple Sclerosis
Ramgolam V, Sha Y, Marcus K, Choudhary N, Troiani L, Chopra M, Markovic-Plese S. B Cells as a Therapeutic Target for IFN-β in Relapsing–Remitting Multiple Sclerosis. The Journal Of Immunology 2011, 186: 4518-4526. PMID: 21368231, DOI: 10.4049/jimmunol.1000271.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsRR-MS patientsIFN-β-1bRelapsing-remitting multiple sclerosisCell stimulatory capacityStimulatory capacityB cellsMS patientsUntreated patientsIL-23IL-27IL-12Multiple sclerosisIL-1βProliferative responseAg-specific T cell proliferative responsesFirst-line immunomodulatory therapyT cell proliferative responsesSuppression of CD40Low proliferative responseB-cell secretionCell proliferative responsesB cell functionMHC class IRR-MSImmunomodulatory therapy
2010
Interferon-beta inhibits Th17 cell differentiation in patients with multiple sclerosis.
Ramgolam V, Markovic-Plese S. Interferon-beta inhibits Th17 cell differentiation in patients with multiple sclerosis. Endocrine Metabolic & Immune Disorders - Drug Targets 2010, 10: 161-7. PMID: 20384573, DOI: 10.2174/187153010791213029.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsDendritic cellsT cellsB cellsMultiple sclerosisCell-mediated autoimmune responseRetinoic acid-related orphan receptorTranscription factor retinoic acid-related orphan receptorAcid-related orphan receptorCytokines IL-17AFirst-line therapyCytokines IL-1bInduction of suppressorCell differentiationMechanism of actionRR-MSIL-17AIL-23Th17 cellsIL-10Immunoregulatory mechanismsIL-12Autoimmune responseAutoimmune diseasesCytokines interleukinChemokine receptors
2009
IFN-β Inhibits Human Th17 Cell Differentiation
Ramgolam V, Sha Y, Jin J, Zhang X, Markovic-Plese S. IFN-β Inhibits Human Th17 Cell Differentiation. The Journal Of Immunology 2009, 183: 5418-5427. PMID: 19783688, DOI: 10.4049/jimmunol.0803227.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsCD4-Positive T-LymphocytesCell DifferentiationCells, CulturedDendritic CellsDown-RegulationHumansInterferon beta-1aInterferon-betaInterleukin-10Interleukin-12 Subunit p35Interleukin-17Interleukin-1betaInterleukin-23 Subunit p19Multiple SclerosisNuclear Receptor Subfamily 1, Group F, Member 3PhosphorylationReceptors, CCR6Receptors, InterleukinReceptors, Retinoic AcidReceptors, Thyroid HormoneSTAT1 Transcription FactorSTAT3 Transcription FactorT-Lymphocytes, Helper-InducerUp-RegulationConceptsTh17 cell differentiationDendritic cellsMultiple sclerosisT cellsReceptor CIL-17AAutoimmune responseIL-1betaIFN beta-1a treatmentRelapsing-remitting multiple sclerosisIL-10 gene expressionTh17 cell markersUntreated MS patientsCNS inflammatory diseasesIL-10 secretionNaive T cellsTh17-polarizing conditionsEffect of IFNCell differentiationIL-27p28 expressionPrimary therapySuppressor of cytokineIL-17IL-23IL-23p19Self-complementary AAV Virus (scAAV) Safe and Long-term Gene Transfer in the Trabecular Meshwork of Living Rats and Monkeys
Buie L, Rasmussen C, Porterfield E, Ramgolam V, Choi V, Markovic-Plese S, Samulski R, Kaufman P, Borrás T. Self-complementary AAV Virus (scAAV) Safe and Long-term Gene Transfer in the Trabecular Meshwork of Living Rats and Monkeys. Investigative Ophthalmology & Visual Science 2009, 51: 236-248. PMID: 19684004, PMCID: PMC2869048, DOI: 10.1167/iovs.09-3847.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAnimalsDependovirusEnzyme-Linked Immunosorbent AssayFemaleFluorescein AngiographyFluorescent Antibody Technique, IndirectGene ExpressionGene Transfer TechniquesGenetic VectorsGonioscopyGreen Fluorescent ProteinsIntraocular PressureMacaca fascicularisMaleOligonucleotide Array Sequence AnalysisRatsRats, Inbred BNRats, WistarReverse Transcriptase Polymerase Chain ReactionTonometry, OcularTrabecular MeshworkTransduction, GeneticConceptsHuman trabecular meshwork cellsTrabecular meshworkIntraocular pressureImmune responseCell-mediated immune responsesAnterior segment tissuesLow immune responseGene therapyTrabecular meshwork cellsSingle doseSingle dosesAAV vectorsCynomolgus monkeysFaster onsetGoldmann tonometerTransgene expressionLong-term gene transferRatsSegment tissuesProliferation assaysAdverse effectsMeshwork cellsSafe deliveryLiving ratsMonkeys
2008
Simvastatin Inhibits IL-17 Secretion by Targeting Multiple IL-17-Regulatory Cytokines and by Inhibiting the Expression of IL-17 Transcription Factor RORC in CD4+ Lymphocytes
Zhang X, Jin J, Peng X, Ramgolam V, Markovic-Plese S. Simvastatin Inhibits IL-17 Secretion by Targeting Multiple IL-17-Regulatory Cytokines and by Inhibiting the Expression of IL-17 Transcription Factor RORC in CD4+ Lymphocytes. The Journal Of Immunology 2008, 180: 6988-6996. PMID: 18453621, DOI: 10.4049/jimmunol.180.10.6988.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsBlotting, WesternCD4-Positive T-LymphocytesCytokinesEnzyme-Linked Immunosorbent AssayFemaleFlow CytometryGene ExpressionHumansImmunologic FactorsInterleukin-17MaleMonocytesMultiple SclerosisNuclear ProteinsOligonucleotide Array Sequence AnalysisReceptors, Cytoplasmic and NuclearReverse Transcriptase Polymerase Chain ReactionSimvastatinSuppressor of Cytokine Signaling 3 ProteinSuppressor of Cytokine Signaling ProteinsT-Lymphocyte SubsetsConceptsAutoimmune responseMultiple sclerosisImmunomodulatory mechanismsT cellsIL-23 gene expressionTranscription factor RORCIL-17 productionIL-17 secretionIL-27 productionChronic inflammatory diseaseNovel immunomodulatory mechanismGood safety profileIL-17 transcriptionPromising therapeutic approachCholesterol-lowering agentsHuman autoimmune responseImmunomodulatory agentsSafety profileAutoimmune diseasesIL-6IL-4Inflammatory diseasesSpecific effectsTherapeutic approachesIFN-gammaDegenerate TCR recognition and dual DR2 restriction of autoreactive T cells: Implications for the initiation of the autoimmune response in multiple sclerosis
Zhang X, Tang Y, Sujkowska D, Wang J, Ramgolam V, Sospedra M, Adams J, Martin R, Pinilla C, Markovic‐Plese S. Degenerate TCR recognition and dual DR2 restriction of autoreactive T cells: Implications for the initiation of the autoimmune response in multiple sclerosis. European Journal Of Immunology 2008, 38: 1297-1309. PMID: 18412170, DOI: 10.1002/eji.200737519.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdolescentAdultAmino Acid SequenceAutoimmunityClone CellsEpitopes, T-LymphocyteHLA-DR2 AntigenHumansInterferon-gammaInterleukin-17Interleukin-4Leukocytes, MononuclearLymphocyte ActivationMiddle AgedMultiple Sclerosis, Relapsing-RemittingMyelin Basic ProteinMyelin ProteinsMyelin Proteolipid ProteinMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinPeptide FragmentsPeptidesReceptors, Antigen, T-CellT-Lymphocyte SubsetsT-LymphocytesConceptsMultiple sclerosisAutoimmune responseT cellsProliferative responseTCR degeneracyMHC class II allelesAutoreactive T cellsClass II allelesT cell activationMyelin peptidesMS patientsDR2 allelesHealthy controlsReactive cellsStimulatory potencyCell activationTCR recognitionCaucasian populationContext of diseaseSclerosisDR2aCellsILTCRPeptidesLFA‐1 engagement‐induced T cell cytokine mRNA stabilization involves a Rac, p38 MAP kinase, MK2 cascade
Rao G, Ramgolam V, DeGregorio S, Chi H, Flavell R, Gaestel M, Collinge M, Bender J. LFA‐1 engagement‐induced T cell cytokine mRNA stabilization involves a Rac, p38 MAP kinase, MK2 cascade. The FASEB Journal 2008, 22: 1070.14-1070.14. DOI: 10.1096/fasebj.22.1_supplement.1070.14.Peer-Reviewed Original ResearchInterferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS)
Ramgolam V, Speer D, Markovic‐Plese S. Interferon (IFN) beta ‐1a induces IL‐27 and IL‐12, and down‐regulates IL‐23 and IL‐1beta in dendritic cells (DCs), establishing inhibitory conditions for Th‐17 cell differentiation: Implications for treatment of multiple sclerosis (MS). The FASEB Journal 2008, 22: 1074.8-1074.8. DOI: 10.1096/fasebj.22.1_supplement.1074.8.Peer-Reviewed Original ResearchConceptsIFN beta-1aDendritic cellsIL-27Beta-1aMultiple sclerosisIL-23IL-1 betaIL-1betaPathogenesis of MSIL-23 promotesIL-27 expressionTh-17 cellsMature dendritic cellsInterferon beta-1aIL-1B expressionCytokines IL-6Cytokine gene expressionInduction of SOCS3Cell differentiationSTAT-1 activationExpression of SOCS3STAT-1 geneQuantitative RT-PCRMS patientsStandard therapy
2005
Inflammatory mechanisms in vascular disease
Mehra V, Ramgolam V, Bender J. Inflammatory mechanisms in vascular disease. Drug Discovery Today Disease Mechanisms 2005, 2: 77-84. DOI: 10.1016/j.ddmec.2005.05.010.Peer-Reviewed Original Research
News
Copy Link
Get In Touch
Copy Link