Ping-Xia Zhang, MD, PhD
Associate Research Scientist in Laboratory MedicineDownloadHi-Res Photo
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Laboratory Medicine
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Laboratory Medicine
PO Box 208035, 333 Cedar Street
New Haven, CT 06520-8035
United States
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Associate Research Scientist in Laboratory Medicine
Biography
Ping-Xia Zhang, Associate Research Scientist, is a senior member of the Krause laboratory with wide research interests and extraordinary technical expertise. Dr. Zhang moved to the United States from China, where she was educated as an MD and then pursued a PhD in Immunology. She next performed postdoctoral studies in Immunology in the Department of Pediatrics at Yale School of Medicine. She then joined the Krause laboratory, where she performed studies in collaboration with Dr. Emanuela Bruscia on cystic fibrosis. She currently divides her time between the laboratories of Drs. Krause and Bruscia, where she provides critical expertise to many ongoing studies and help students and postdocs to complete their projects in both laboratories.
Last Updated on August 12, 2026.
Appointments
Laboratory Medicine
Associate Research ScientistPrimary
Other Departments & Organizations
- Bruscia Lab
- Laboratory Medicine
Education & Training
- Postdoc
- Yale University School of Medicine (1999)
- PhD
- Beijing Medical University, Immunology (1995)
- MD
- Henan Medical University, P.R.C. (1983)
Research
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Research at a Glance
Yale Co-Authors
Frequent collaborators of Ping-Xia Zhang's published research.
Publications Timeline
A big-picture view of Ping-Xia Zhang's research output by year.
Diane Krause, MD, PhD
Emanuela Bruscia, PhD
Marie Egan, MD
Thomas Murray, MD, PhD
Caterina Di Pietro
Former YSMAnjelica Gonzalez, PhD
7Publications
493Citations
Publications
2024
Ezrin drives adaptation of monocytes to the inflamed lung microenvironment
Gudneppanavar R, Di Pietro C, H Öz H, Zhang P, Cheng E, Huang P, Tebaldi T, Biancon G, Halene S, Hoppe A, Kim C, Gonzalez A, Krause D, Egan M, Gupta N, Murray T, Bruscia E. Ezrin drives adaptation of monocytes to the inflamed lung microenvironment. Cell Death & Disease 2024, 15: 864. PMID: 39613751, PMCID: PMC11607083, DOI: 10.1038/s41419-024-07255-8.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsActivation of focal adhesion kinaseExtracellular matrixActin-binding proteinsFocal adhesion kinaseLung extracellular matrixKnock-out mouse modelProtein Kinase SignalingCortical cytoskeletonLoss of ezrinKinase signalingPlasma membraneCell migrationSignaling pathwayEzrinResponse to lipopolysaccharideTissue-resident macrophagesMouse modelLipopolysaccharideCytoskeletonEzrin expressionLung microenvironmentKinaseMonocyte recruitmentProteinAktCDK9 phosphorylates RUNX1 to promote megakaryocytic fate in megakaryocytic-erythroid progenitors
Kwon N, Lu Y, Thompson E, Mancuso R, Wang L, Zhang P, Krause D. CDK9 phosphorylates RUNX1 to promote megakaryocytic fate in megakaryocytic-erythroid progenitors. Blood 2024, 144: 1800-1812. PMID: 39102635, PMCID: PMC11530366, DOI: 10.1182/blood.2024023963.Peer-Reviewed Original ResearchCitationsAltmetricConceptsMegakaryocytic-erythroid progenitorsWild-typeFate specificationRUNX1 levelsCell lines expressing wild-typeHuman erythroleukemiaInhibition of CDK9Cell-type specific transcription factorsMK-specificRUNX1 variantsDifferentially regulates expressionErythroid commitmentHematopoietic homeostasisHuman erythroleukemia cellsMK progenitorsOverexpression of RUNX1Megakaryocyte fateDecreased expressionRUNX1Mimetic mutationNon-phosphorylatableTranscription machineryFunctional efficacySerine/threonine phosphorylationSerine/threonine kinaseCCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and cystic fibrosis mice
Öz H, Braga C, Gudneppanavar R, Di Pietro C, Huang P, Zhang P, Krause D, Egan M, Murray T, Bruscia E. CCR2+ monocytes are dispensable to resolve acute pulmonary Pseudomonas aeruginosa infections in WT and cystic fibrosis mice. Journal Of Leukocyte Biology 2024, 117: qiae218. PMID: 39365279, PMCID: PMC11953069, DOI: 10.1093/jleuko/qiae218.Peer-Reviewed Original ResearchCitationsConceptsLung tissue damageCystic fibrosisTissue damageMonocyte recruitmentImmune responsePulmonary Pseudomonas aeruginosa infectionHyper-inflammatory immune responseCystic fibrosis micePropagate tissue damagePseudomonas aeruginosaLungs of patientsChronic neutrophilic inflammationImmunological response to infectionHost immune responseMonocyte-derived macrophagesTarget monocyte recruitmentSite of injuryResponse to infectionCFTR modulatorsPA infectionChronic inflammatory disease conditionsReduced bactericidal activityAdjunctive therapyClinical outcomesEradicate infection
2015
Pharmacological modulation of the AKT/microRNA-199a-5p/CAV1 pathway ameliorates cystic fibrosis lung hyper-inflammation
Zhang PX, Cheng J, Zou S, D'Souza AD, Koff JL, Lu J, Lee PJ, Krause DS, Egan ME, Bruscia EM. Pharmacological modulation of the AKT/microRNA-199a-5p/CAV1 pathway ameliorates cystic fibrosis lung hyper-inflammation. Nature Communications 2015, 6: 6221. PMID: 25665524, PMCID: PMC4324503, DOI: 10.1038/ncomms7221.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsCF macrophagesMiR-199aMicroRNA-199aHyper-inflammatory responseCFTR-deficient miceCystic fibrosis patientsCystic fibrosis lungLung destructionDisease morbidityPharmacological modulationCF miceCF lungFibrosis patientsInnate immunityLungMacrophagesCAV1 expressionDrug celecoxibReduced levelsTLR4CelecoxibMiceCav1PathwayMorbidity
2013
Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator
Zhang PX, Murray TS, Villella VR, Ferrari E, Esposito S, D'Souza A, Raia V, Maiuri L, Krause DS, Egan ME, Bruscia EM. Reduced Caveolin-1 Promotes Hyperinflammation due to Abnormal Heme Oxygenase-1 Localization in Lipopolysaccharide-Challenged Macrophages with Dysfunctional Cystic Fibrosis Transmembrane Conductance Regulator. The Journal Of Immunology 2013, 190: 5196-5206. PMID: 23606537, PMCID: PMC3711148, DOI: 10.4049/jimmunol.1201607.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdolescentAdultAnimalsCaveolin 1Cells, CulturedChildChild, PreschoolCystic FibrosisCystic Fibrosis Transmembrane Conductance RegulatorFemaleHeme Oxygenase-1HumansInflammationLipopolysaccharidesLung DiseasesMacrophagesMaleMembrane ProteinsMiceMice, KnockoutNasal PolypsReactive Oxygen SpeciesSignal TransductionToll-Like Receptor 4Young AdultConceptsCav-1 expressionHeme oxygenase-1Dysfunctional cystic fibrosis transmembrane conductance regulatorCystic fibrosis transmembrane conductance regulatorCell surfaceFibrosis transmembrane conductance regulatorProtein caveolin-1Cellular redox statusCell surface localizationCellular oxidative stateTransmembrane conductance regulatorHO-1 enzymePositive feed-forward loopCystic fibrosis macrophagesNegative regulatorCaveolin-1Conductance regulatorCell survivalHO-1 deliverySurface localizationRedox statusMΦ responsesHO-1/CO pathwayPathwayPotential target
2011
Abnormal Trafficking and Degradation of TLR4 Underlie the Elevated Inflammatory Response in Cystic Fibrosis
Bruscia EM, Zhang PX, Satoh A, Caputo C, Medzhitov R, Shenoy A, Egan ME, Krause DS. Abnormal Trafficking and Degradation of TLR4 Underlie the Elevated Inflammatory Response in Cystic Fibrosis. The Journal Of Immunology 2011, 186: 6990-6998. PMID: 21593379, PMCID: PMC3111054, DOI: 10.4049/jimmunol.1100396.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and Concepts
2009
Macrophages Directly Contribute to the Exaggerated Inflammatory Response in Cystic Fibrosis Transmembrane Conductance Regulator−/− Mice
Bruscia EM, Zhang PX, Ferreira E, Caputo C, Emerson JW, Tuck D, Krause DS, Egan ME. Macrophages Directly Contribute to the Exaggerated Inflammatory Response in Cystic Fibrosis Transmembrane Conductance Regulator−/− Mice. American Journal Of Respiratory Cell And Molecular Biology 2009, 40: 295-304. PMID: 18776130, PMCID: PMC2645527, DOI: 10.1165/rcmb.2008-0170oc.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsExaggerated inflammatory responseExaggerated immune responseBone marrow-derived macrophagesIL-6Marrow-derived macrophagesCystic fibrosisCF miceKeratinocyte chemoattractantCytokine responsesInflammatory responseIL-1alphaImmune responseAlveolar macrophagesBronchoalveolar lavage fluidGranulocyte colony-stimulating factorNumber of neutrophilsChemoattractant protein-1CF lung diseaseElevated cytokine responseInnate immune systemImportant therapeutic targetCF mouse modelsPopulation of macrophagesColony-stimulating factorPseudomonas aeruginosa LPS
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Laboratory Medicine
PO Box 208035, 333 Cedar Street
New Haven, CT 06520-8035
United States