Seth Guller, PhD
Senior Research Scientist in Obstetrics, Gynecology, and Reproductive SciencesDownloadHi-Res Photo
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Appointments
Additional Titles
Director, Gyn/Endocrine Laboratory
Contact Info
Obstetrics, Gynecology & Reproductive Sciences
333 Cedar Street
New Haven, CT 06510-
United States
Appointments
Additional Titles
Director, Gyn/Endocrine Laboratory
Contact Info
Obstetrics, Gynecology & Reproductive Sciences
333 Cedar Street
New Haven, CT 06510-
United States
Appointments
Additional Titles
Director, Gyn/Endocrine Laboratory
Contact Info
Obstetrics, Gynecology & Reproductive Sciences
333 Cedar Street
New Haven, CT 06510-
United States
About
Titles
Senior Research Scientist in Obstetrics, Gynecology, and Reproductive Sciences
Director, Gyn/Endocrine Laboratory
Biography
Dr. Seth Guller, trained as a biochemist, joined the Yale Fertility Center as Director of the Reproductive Endocrinology Laboratory in 2007. The function of this clinical laboratory is to provide rapid hormone analysis for patients as well as test results for research studies. Dr. Guller strives to implement new tests for the recently acquired Roche Cobas e411 analyzer to improve the quality of patient care. He has also directed a research laboratory for the last 21 years. Dr. Guller has published more than 75 peer-reviewed papers.
Appointments
Obstetrics, Gynecology & Reproductive Sciences
Senior Research ScientistPrimary
Other Departments & Organizations
- Discovery to Cure Internship
- Fertility Center
- Guller Lab
- Obstetrics, Gynecology & Reproductive Sciences
- Perinatal Research
- Reproductive Endocrinology & Infertility
- Reproductive Sciences
Education & Training
- PhD
- Mount Sinai School of Medicine (1986)
Research
Overview
Medical Subject Headings (MeSH)
Gynecology; Obstetrics; Placenta Diseases; Pre-Eclampsia; Pregnancy Outcome
Research at a Glance
Yale Co-Authors
Frequent collaborators of Seth Guller's published research.
Publications Timeline
A big-picture view of Seth Guller's research output by year.
Research Interests
Research topics Seth Guller is interested in exploring.
Charles Lockwood, MD
Harvey Kliman, MD, PhD
Vikki M Abrahams, PhD
Erol Fikrig, MD
Liubin Yang, MD, PhD, FACOG
Mancy Tong, PhD
79Publications
4,778Citations
Pre-Eclampsia
Placenta Diseases
Pregnancy Outcome
Publications
2023
Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis
Ozmen A, Nwabuobi C, Tang Z, Guo X, Larsen K, Guller S, Blas J, Moore M, Kayisli U, Lockwood C, Guzeloglu-Kayisli O. Leptin-Mediated Induction of IL-6 Expression in Hofbauer Cells Contributes to Preeclampsia Pathogenesis. International Journal Of Molecular Sciences 2023, 25: 135. PMID: 38203306, PMCID: PMC10778808, DOI: 10.3390/ijms25010135.Peer-Reviewed Original ResearchMeSH Keywords and ConceptsConceptsIL-6 expressionHofbauer cellsP65 NF-κBIL-6NF-κBLeptin levelsPreeclampsia pathogenesisElevated serum interleukin-6 levelsSerum interleukin-6 levelsERK1/2 MAPKInterleukin-6 levelsPro-inflammatory phenotypeAnti-inflammatory phenotypeLeptin receptor expressionIL-6 productionPathogenesis of PEPlacental leptin productionPhosphorylation levelsERK1/2 MAPK inhibitorIL-6 regulationConcentration-dependent mannerPE patientsHuman pregnancySecond trimesterLeptin concentrations
2022
Insulin increases placental triglyceride as a potential mechanism for fetal adiposity in maternal obesity
Anam AK, Cooke KM, Dratver MB, O'Bryan JV, Perley LE, Guller SM, Hwang JJ, Taylor HS, Goedeke L, Kliman HJ, Vatner DF, Flannery CA. Insulin increases placental triglyceride as a potential mechanism for fetal adiposity in maternal obesity. Molecular Metabolism 2022, 64: 101574. PMID: 35970449, PMCID: PMC9440306, DOI: 10.1016/j.molmet.2022.101574.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsDe novo lipogenesisFetal adiposityFatty acid uptakeMaternal obesityObese womenNormal weightExcess adiposityVillous explantsInsulin receptorNewborns of mothersNormal-weight womenAcid uptakePlacental villous explantsTranscription factor SREBP-1Insulin-like growth factor 2Effect of insulinFatty acid oxidationPlacental triglyceridesPlacental responsesElevated triglyceridesMaternal hyperglycemiaWeight womenGrowth factor 2Diabetes riskPlacental metabolism
2021
YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion
Feliciano D, Ott CM, Espinosa-Medina I, Weigel AV, Benedetti L, Milano KM, Tang Z, Lee T, Kliman HJ, Guller SM, Lippincott-Schwartz J. YAP1 nuclear efflux and transcriptional reprograming follow membrane diminution upon VSV-G-induced cell fusion. Nature Communications 2021, 12: 4502. PMID: 34301937, PMCID: PMC8302681, DOI: 10.1038/s41467-021-24708-2.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsMeSH KeywordsAdaptor Proteins, Signal TransducingAMP-Activated Protein KinasesAnimalsBiological TransportCell FusionCell LineCell Line, TumorCell MembraneCell NucleusCells, CulturedGiant CellsHEK293 CellsHumansMembrane GlycoproteinsMiceRNA-SeqSignal TransductionTranscription FactorsTranscription, GeneticViral Envelope ProteinsYAP-Signaling ProteinsConceptsCell cycle arrestCell fusionNew cellular statesPlasma membrane surface areaRNA-seq analysisCell fusion systemTranscriptional programsNutrient stressCellular statesTranscriptional changesNuclear effluxCytoplasmic glucoseExtrinsic cuesUndifferentiated cellsGlucose transporterFused cellsMechanistic insightsMembrane surface areaNew functionsEndocytosisYAP1 inhibitionEnergetic stateSyncytiaCellsVSVMaternal respiratory SARS-CoV-2 infection in pregnancy is associated with a robust inflammatory response at the maternal-fetal interface
Lu-Culligan A, Chavan AR, Vijayakumar P, Irshaid L, Courchaine EM, Milano KM, Tang Z, Pope SD, Song E, Vogels CBF, Lu-Culligan WJ, Campbell KH, Casanovas-Massana A, Bermejo S, Toothaker JM, Lee HJ, Liu F, Schulz W, Fournier J, Muenker MC, Moore AJ, Team Y, Konnikova L, Neugebauer KM, Ring A, Grubaugh ND, Ko AI, Morotti R, Guller S, Kliman HJ, Iwasaki A, Farhadian SF. Maternal respiratory SARS-CoV-2 infection in pregnancy is associated with a robust inflammatory response at the maternal-fetal interface. Med 2021, 2: 591-610.e10. PMID: 33969332, PMCID: PMC8084634, DOI: 10.1016/j.medj.2021.04.016.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSARS-CoV-2 infectionMaternal-fetal interfaceACE2 expressionNatural killerPregnant womenPlacental cellsAcute respiratory syndrome coronavirus 2 infectionSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) infectionSARS-CoV-2-infected womenTerm placentaSyndrome coronavirus 2 infectionCoronavirus 2 infectionPotential immune mechanismsRobust inflammatory responseRobust immune responseCoronavirus disease 2019Detectable viral RNAInterferon-related genesLower ACE2 expressionMajority of placentasPregnancy complicationsPlacental histologyHofbauer cellsEarly pregnancyImmune activation
2020
Acetaminophen Attenuates invasion and alters the expression of extracellular matrix enzymes and vascular factors in human first trimester trophoblast cells
Burman A, Garcia-Milian R, Wood M, DeWitt NA, Vasiliou V, Guller S, Abrahams VM, Whirledge S. Acetaminophen Attenuates invasion and alters the expression of extracellular matrix enzymes and vascular factors in human first trimester trophoblast cells. Placenta 2020, 104: 146-160. PMID: 33348283, DOI: 10.1016/j.placenta.2020.12.002.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsFirst trimester trophoblast cellsHuman first trimester trophoblast cellsPrenatal acetaminophen useTrophoblast cellsAcetaminophen useTrophoblast functionsAcetaminophen exposureFetal developmentHTR-8/SVneo cellsPrenatal acetaminophen exposureAnti-inflammatory drug aspirinRecent epidemiological studiesPlacental cell typesMatrix metalloproteinases 2Expression of angiogenesisExtracellular matrix enzymesPrenatal acetaminophenCommon medicationsVascular factorsMaternal healthPlacental functionEpidemiological associationLong-term effectsCyclooxygenase-1Epidemiological studiesZika Virus-Infected Decidual Cells Elicit a Gestational Age-Dependent Innate Immune Response and Exaggerate Trophoblast Zika Permissiveness: Implication for Vertical Transmission.
Guzeloglu-Kayisli O, Guo X, Tang Z, Semerci N, Ozmen A, Larsen K, Mutluay D, Guller S, Schatz F, Kayisli UA, Lockwood CJ. Zika Virus-Infected Decidual Cells Elicit a Gestational Age-Dependent Innate Immune Response and Exaggerate Trophoblast Zika Permissiveness: Implication for Vertical Transmission. The Journal Of Immunology 2020, 205: 3083-3094. PMID: 33139490, DOI: 10.4049/jimmunol.2000713.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHuman decidual cellsDecidual cellsZika virusViral attachment factorsTerm decidual stromal cellsVertical transmissionDecidual cell supernatantsTerm decidual cellsInnate immune response genesInnate immune responsivenessExact pathogenic mechanismDecidual stromal cellsHuman first trimesterInnate immune responseSevere fetal defectsImmune response genesFetal sequelaeGestational ageFirst trimesterPlacental transmissionZIKV infectionCytotrophoblast culturesImmune responsivenessZika infectionLate pregnancyPeri‐implantation cytokine profile differs between singleton and twin IVF pregnancies
Simpson S, Kaislasuo J, Peng G, Aldo P, Paidas M, Guller S, Mor G, Pal L. Peri‐implantation cytokine profile differs between singleton and twin IVF pregnancies. American Journal Of Reproductive Immunology 2020, 85: e13348. PMID: 32946159, PMCID: PMC8221280, DOI: 10.1111/aji.13348.Peer-Reviewed Original ResearchCitationsMeSH Keywords and ConceptsConceptsMaternal serum levelsSerum levelsSingleton gestationsIL-10Twin pregnanciesC motif chemokine ligand 10General immune reactionTwin IVF pregnanciesProspective longitudinal cohortSerum cytokine concentrationsAcademic fertility centerSerial serum samplesChemokine ligand 10Implantation phaseAnti-angiogenic roleSingleton conceptionsCXCL10 levelsIVF pregnanciesIVF-ETCytokine concentrationsInterleukin-10Fertility centerSerum concentrationsTumor necrosisLongitudinal cohortNLRP3 inflammasome function and pyroptotic cell death in human placental Hofbauer cells
Abrahams VM, Tang Z, Mor G, Guller S. NLRP3 inflammasome function and pyroptotic cell death in human placental Hofbauer cells. Journal Of Reproductive Immunology 2020, 142: 103214. PMID: 33152658, PMCID: PMC7770077, DOI: 10.1016/j.jri.2020.103214.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHofbauer cellsCaspase-1 activationIL-1β processingIL-1βInflammasome activationFetal inflammatory response syndromeSubsequent pregnancy complicationsInflammatory response syndromeCell deathNLRP3 inflammasome activationInterleukin-1 betaIL-1β secretionInhibition of P2X7Human term placentaGasdermin D cleavageNLRP3 knockdownPlacental inflammationPyroptotic cell deathFetal inflammationHistologic chorioamnionitisPregnancy complicationsResponse syndromeNLRP3 inflammasomeProtein/gene expressionInflammatory formTrophoblast-secreted soluble-PD-L1 modulates macrophage polarization and function
Zhang Y, Aldo P, You Y, Ding J, Kaislasuo J, Petersen JF, Lokkegaard E, Peng G, Paidas MJ, Simpson S, Pal L, Guller S, Liu H, Liao AH, Mor G. Trophoblast-secreted soluble-PD-L1 modulates macrophage polarization and function. Journal Of Leukocyte Biology 2020, 108: 983-998. PMID: 32386458, PMCID: PMC8190653, DOI: 10.1002/jlb.1a0420-012rr.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsSoluble PD-L1Macrophage polarizationTrophoblast cellsCell death ligand 1PD-L1/PDPD-1 blockageDeath ligand 1Macrophage differentiationModulates macrophage polarizationExpression/secretionDecidual macrophagesHealthy pregnancyPD-L1Pregnant womenTLR4 ligationM2 phenotypeExpression of typeFetal developmentLPS activationMacrophagesIFNPlacenta developmentLigand 1Constitutive productionGestationHuman Chorionic Gonadotropin modulates CXCL10 Expression through Histone Methylation in human decidua
Silasi M, You Y, Simpson S, Kaislasuo J, Pal L, Guller S, Peng G, Ramhorst R, Grasso E, Etemad S, Durosier S, Aldo P, Mor G. Human Chorionic Gonadotropin modulates CXCL10 Expression through Histone Methylation in human decidua. Scientific Reports 2020, 10: 5785. PMID: 32238853, PMCID: PMC7113245, DOI: 10.1038/s41598-020-62593-9.Peer-Reviewed Original ResearchCitationsAltmetricMeSH Keywords and ConceptsConceptsHuman chorionic gonadotropinCXCL10 expressionChorionic gonadotropinPotent immune-modulatory effectsImmune system undergoesImmune modulatory effectsEndometrial stromal cellsImmune cell recruitmentMaternal-fetal interfaceImmune regulatory functionsProcess of implantationCD8 cellsCytokine profilePregnancy progressesFetal interfaceDecidual samplesImmune populationsImmune factorsHuman deciduaT cellsDecidual cellsCell recruitmentModulatory effectsEarly hormoneStromal cells
News
News
- August 18, 2016
Yale study identifies how Zika virus infects the placenta
- August 18, 2016
Yale study identifies how Zika virus infects the placenta
- March 15, 2007
In Preeclampsia, Researchers Identify Proteins that Cause Blood Vessel Damage
- February 28, 2005
Proteins Found in Urine of Pregnant Women Could Help Diagnose Preeclampsia
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Obstetrics, Gynecology & Reproductive Sciences
333 Cedar Street
New Haven, CT 06510-
United States