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Instructor
Biography
Dr. Sharma was recruited to the Adams Center from Harvard in 2024. She is Instructor and Faculty at Yale School of Medicine. Dr. Sharma earned a master’s degree in biotechnology with an additional research training from the Institute of Genomics and Integrative Biology in India. She pursued doctoral studies at the University of Alberta, Canada, under the mentorship of Prof. Patrick Flood.
Dr. Sharma’s doctoral research centered on elucidating the role of beta2-adrenergic receptor (β2-AR) activation in modulating microglial response during neuro-inflammatory conditions in Parkinson’s disease. Her findings showed the underlying mechanism by which β2-AR agonists regulate microglia activation and neuroinflammation (Sharma et al, 2018). She also identified the specific pathways involved in the anti-inflammatory conversion of activated microglia by β2-AR agonists (Sharma et al, 2019).
At Harvard Medical School, Dr. Sharma evaluated the role of β2-AR activation in Parkinson’s disease. In 2024 she joined the Adams Center at Yale. Her research investigates the role of beta2- adrenoreceptor agonists in regulating mitochondrial function and synucleinopathy.
Dr. Sharma’s significant contributions have been recognized through prestigious fellowships from the Parkinson’s Association of Alberta, Canada, and the American Parkinson’s Disease Association (APDA).
Appointments
Education & Training
- Postdoctoral Fellow
- Brigham and Women's Hospital, Harvard Medical School
- PhD
- University of Alberta, Immunology
Research
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Overview
Medical Research Interests
ORCID
0000-0002-7258-1399- View Lab Website
Scherzer Lab
Research at a Glance
Research Interests
Inflammation
Publications
2021
Impact of a CD36 inhibitor on Porphyromonas gingivalis mediated atherosclerosis
Rekhi U, Catunda R, Alexiou M, Sharma M, Fong A, Febbraio M. Impact of a CD36 inhibitor on Porphyromonas gingivalis mediated atherosclerosis. Archives Of Oral Biology 2021, 126: 105129. PMID: 33934042, DOI: 10.1016/j.archoralbio.2021.105129.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsMarkers of inflammationPeriodontal diseaseP. gingivalisCD36 inhibitorBone lossCytokine arrayMicro-CT measurementsLow-density lipoprotein receptor knockoutMeasurement of bone lossP. gingivalis lipopolysaccharideNF-kBMale LDLr-KO miceExpression of pro-inflammatory cytokinesLDLr-KO miceRAW-Blue macrophagesPro-inflammatory cytokinesLevels of plasma cholesterolMicro-CTNF-kB activationPorphyromonas gingivalisReceptor knockoutTreated miceKO miceOral lavageIn vitro analysis
2019
Adrenergic Receptors as Pharmacological Targets for Neuroinflammation and Neurodegeneration in Parkinson’s Disease
Sharma M, M. Flood P. Adrenergic Receptors as Pharmacological Targets for Neuroinflammation and Neurodegeneration in Parkinson’s Disease. 2019 DOI: 10.5772/intechopen.81343.ChaptersCitationsMechanism underlying β2-AR agonist-mediated phenotypic conversion of LPS-activated microglial cells
Sharma M, Arbabzada N, Flood P. Mechanism underlying β2-AR agonist-mediated phenotypic conversion of LPS-activated microglial cells. Journal Of Neuroimmunology 2019, 332: 37-48. PMID: 30933849, DOI: 10.1016/j.jneuroim.2019.03.017.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdrenergic beta-2 Receptor AgonistsAnimalsBiomarkersCell LineCyclic AMP Response Element-Binding ProteinCytokinesEndotoxinsGene Expression RegulationInflammationInterleukin-10MAP Kinase Signaling SystemMiceMicrogliaPhenotypePhosphatidylinositol 3-KinasesReactive Oxygen SpeciesRNA InterferenceSalmeterol XinafoateSignal TransductionConceptsM2-like phenotypeMurine microglial BV2 cellsPhenotypic conversionTranscription factor CREBBV2 cellsLPS-activated microgliaMAPK signaling pathwayP38 MAPK signaling pathwayIL-10LPS-activated BV2 cellsReactive oxygen speciesSiRNA approachMicroglial BV2 cellsProduction of IL-10Signaling pathwayB2-ARTumor necrosis factor-aExpression of arginase-1PI3KB2 adrenergic receptorLPS-activated microglial cellsCytokine IL-10Neurodegenerative diseasesLPS-induced mediatorsTreatment of neuroinflammatory diseases
2018
β-arrestin2 regulates the anti-inflammatory effects of Salmeterol in lipopolysaccharide-stimulated BV2 cells
Sharma M, Flood P. β-arrestin2 regulates the anti-inflammatory effects of Salmeterol in lipopolysaccharide-stimulated BV2 cells. Journal Of Neuroimmunology 2018, 325: 10-19. PMID: 30352316, DOI: 10.1016/j.jneuroim.2018.10.001.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsEffects of salmeterolAnti-inflammatory effectsPro-inflammatory mediatorsAnti-inflammatory propertiesNeuronal lossAnimal modelsMicroglial activationTumor necrosis factor-aAnimal models of PDBV2 cellsB2 adrenergic receptorNuclear translocationNuclear factor kappa BExpression of pro-inflammatory genesMicroglial cell activationLPS-induced releaseParkinson's diseaseTranslocation of nuclear factor kappa BNuclear translocation of nuclear factor kappa BModel of PDProduction of pro-inflammatory mediatorsFactor kappa BPro-inflammatory genesTAK1-binding proteinChronic inflammationReactive Oxygen Species Mediate Therapeutic Ultrasound-Induced, Mitogen-Activated Protein Kinase Activation in C28/I2 Chondrocytes
Kaur H, Siraki A, Sharma M, Uludağ H, Dederich D, Flood P, El-Bialy T. Reactive Oxygen Species Mediate Therapeutic Ultrasound-Induced, Mitogen-Activated Protein Kinase Activation in C28/I2 Chondrocytes. Ultrasound In Medicine & Biology 2018, 44: 2105-2114. PMID: 30037475, DOI: 10.1016/j.ultrasmedbio.2018.05.025.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsLow-intensity pulsed ultrasoundReactive oxygen species generationOxygen species generationLow-intensity pulsed ultrasound applicationPhosphorylation levels of ERK1/2Phosphorylation levelsSpecies generationLevels of ERK1/2Non-healing fracturesMitogen-activated protein kinase activationReverse transcription polymerase chain reactionProtein kinase activityTranscription polymerase chain reactionMitogen-activated protein kinaseMechanism of actionPolymerase chain reactionQuantitative reverse transcription polymerase chain reactionExpression of SOX9
2017
Salmeterol, a Long‐Acting β2‐Adrenergic Receptor Agonist, Inhibits Macrophage Activation by Lipopolysaccharide From Porphyromonas gingivalis
Sharma M, Patterson L, Chapman E, Flood P. Salmeterol, a Long‐Acting β2‐Adrenergic Receptor Agonist, Inhibits Macrophage Activation by Lipopolysaccharide From Porphyromonas gingivalis. The Journal Of Periodontology 2017, 88: 681-692. PMID: 28398147, DOI: 10.1902/jop.2017.160464.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsMeSH KeywordsAdrenergic beta-2 Receptor AgonistsAnimalsDown-RegulationEnzyme-Linked Immunosorbent AssayHumansInflammationLipopolysaccharidesMacrophage ActivationMiceNF-kappa BNF-KappaB Inhibitor alphap38 Mitogen-Activated Protein KinasesPhosphorylationPorphyromonas gingivalisRAW 264.7 CellsSalmeterol XinafoateTHP-1 CellsConceptsActivation of NF-kBTHP-1 cellsInflammatory responsePorphyromonas gingivalisNF-kBReceptor agonistsMitogen-activated protein kinasePathogenesis of periodontal diseaseReverse-transcriptase polymerase chain reactionTHP-1Murine macrophage cell line RAW264.7Extracellular signal-regulated kinase 1/2Chronic obstructive pulmonary diseaseProduction of proinflammatory mediatorsTLR pathway activationNuclear translocationSignal-regulated kinase 1/2Nuclear factor kappa BProduction of inflammatory mediatorsMacrophage cell line RAW264.7Nuclear translocation of NF-kBEscherichia coli lipopolysaccharideEnzyme-linked immunosorbent assayObstructive pulmonary diseaseTranslocation of NF-kB
2016
Inflammation: Role in Parkinson's Disease and Target for Therapy
Flood P, Arbabzada N, Sharma M. Inflammation: Role in Parkinson's Disease and Target for Therapy. 2016 DOI: 10.5772/63164.ChaptersCitations
Clinical Trials
Current Trials
Yale Harvard Biomarkers Study
HIC ID2000035641RoleSub InvestigatorPrimary Completion Date12/31/2034Recruiting Participants
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101 College Street
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Fl 10
New Haven, CT 06510
300 George Street
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Fl 8, Rm 8104
New Haven, CT 06511