2024
High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish
Seli D, Prendergast A, Ergun Y, Tyagi A, Taylor H. High NaCl Concentrations in Water Are Associated with Developmental Abnormalities and Altered Gene Expression in Zebrafish. International Journal Of Molecular Sciences 2024, 25: 4104. PMID: 38612913, PMCID: PMC11012806, DOI: 10.3390/ijms25074104.Peer-Reviewed Original ResearchConceptsNaCl concentrationGene expressionIncreasing NaCl concentrationATM signaling pathwayUninflated swim bladderSwim bladder developmentHigh NaCl concentrationsEmbryo growthAssociated with developmental abnormalitiesSwim bladderLarval stageEarly embryo growthEmbryonic deathDevelopmental abnormalitiesSignaling pathwayDevelopment of zebrafishGenes SHHCalcium chlorideGenesSodium chlorideE3 mediumStages of developmentZebrafish embryosAffected ecosystemsPotassium chloride
2023
Maternal CXCR4 deletion results in placental defects and pregnancy loss mediated by immune dysregulation
Lyu F, Burzynski C, Fang Y, Tal A, Chen A, Kisa J, Agrawal K, Kluger Y, Taylor H, Tal R. Maternal CXCR4 deletion results in placental defects and pregnancy loss mediated by immune dysregulation. JCI Insight 2023, 8: e172216. PMID: 37815869, PMCID: PMC10721256, DOI: 10.1172/jci.insight.172216.Peer-Reviewed Original ResearchConceptsCXCR4-deficient micePlacental vascular developmentNK cellsCxcr4 deletionNormal placental vascular developmentPlacental developmentNK cell dysfunctionNK cell expressionNK cell infiltrationNK cell functionRole of CXCR4Cell functionMaternal-fetal interfaceImmune cell functionEarly placental developmentWt CXCR4Immune dysregulationVascular developmentGiant cell layerImmune toleranceCXCR4 expressionPeripheral bloodPregnancy failureCell infiltrationPregnancy lossLet-7 suppresses liver fibrosis by inhibiting hepatocyte apoptosis and TGF-β production
Song J, Lv H, Liu B, Hao M, Taylor H, Zhang X, Li D, Huang Y. Let-7 suppresses liver fibrosis by inhibiting hepatocyte apoptosis and TGF-β production. Molecular Metabolism 2023, 78: 101828. PMID: 37898449, PMCID: PMC10641683, DOI: 10.1016/j.molmet.2023.101828.Peer-Reviewed Original ResearchConceptsFas-mediated apoptosisLet-7Hepatocyte apoptosisNegative feedback loopMouse primary hepatocytesLet-7 miRNAsTGF-b signalingSignaling networksApoptosis of hepatocytesTransient transfectionFas expressionInhibiting hepatocyte apoptosisSiRNA knockdownLet-7 expressionLet-7 overexpressionMouse modelApoptosisPrimary hepatocytesSuppressed hepatocyte apoptosisTET3Liver fibrosisFeedback loopExpressionDriver of liver fibrosisAdeno-associated viral vectors
2012
A polymorphism in a let‐7 microRNA binding site of KRAS in women with endometriosis
Grechukhina O, Petracco R, Popkhadze S, Massasa E, Paranjape T, Chan E, Flores I, Weidhaas JB, Taylor HS. A polymorphism in a let‐7 microRNA binding site of KRAS in women with endometriosis. EMBO Molecular Medicine 2012, 4: 206-217. PMID: 22307873, PMCID: PMC3376847, DOI: 10.1002/emmm.201100200.Peer-Reviewed Original ResearchConceptsEndometrial stromal cellsKRAS-variantCultured endometrial stromal cellsStromal cellsAbnormal endometrial growthDe novo endometriosisProgesterone receptor levelsRelatives of womenEndometrial xenograftsKRAS resultsLCS6 polymorphismEndometrial growthReproductive ageKRAS mutationsReceptor levelsMurine modelEndometriosisEndometriosis riskControl populationVariant allelesKRAS mRNAProtein expressionKRASWomenKRAS protein
2011
Novel Therapies Targeting Endometriosis
Taylor HS, Osteen KG, Bruner-Tran KL, Lockwood CJ, Krikun G, Sokalska A, Duleba AJ. Novel Therapies Targeting Endometriosis. Reproductive Sciences 2011, 18: 814-823. PMID: 21693775, PMCID: PMC4046304, DOI: 10.1177/1933719111410713.Peer-Reviewed Original ResearchConceptsNonhuman primate trialsAnti-inflammatory drugsProgesterone modulatorsEndometrial glandsPainful disordersNovel therapiesCommon causeSelective estrogenAntiangiogenic agentsWomen's qualityPotential therapyRodent modelsEndometriosisTherapyDiseaseStem cellsFurther testingPromising new developmentStatinsEstrogenInfertilityUterusStromaTrialsDerivation of Insulin Producing Cells From Human Endometrial Stromal Stem Cells and Use in the Treatment of Murine Diabetes
Santamaria X, Massasa EE, Feng Y, Wolff E, Taylor HS. Derivation of Insulin Producing Cells From Human Endometrial Stromal Stem Cells and Use in the Treatment of Murine Diabetes. Molecular Therapy 2011, 19: 2065-2071. PMID: 21878900, PMCID: PMC3222529, DOI: 10.1038/mt.2011.173.Peer-Reviewed Original ResearchConceptsHuman endometrial stromal stem cellsStromal stem cellsPancreatic islet cell transplantationStem cellsIslet cell transplantationType 1 diabetesBlood glucose levelsTreatment of murineDifferentiated cellsDiabetic miceCell transplantationKidney capsuleCadaveric donorsPotential therapeutic applicationsProgressive hyperglycemiaInsulin secretionMurine modelGlucose levelsUterine endometriumMesenchymal stem cellsΒ-cell markersInsulinHuman insulinGlucose-responsive mannerControl cellsTreatment with Bazedoxifene, a Selective Estrogen Receptor Modulator, Causes Regression of Endometriosis in a Mouse Model
Kulak J, Fischer C, Komm B, Taylor HS. Treatment with Bazedoxifene, a Selective Estrogen Receptor Modulator, Causes Regression of Endometriosis in a Mouse Model. Endocrinology 2011, 152: 3226-3232. PMID: 21586552, PMCID: PMC3138238, DOI: 10.1210/en.2010-1010.Peer-Reviewed Original ResearchConceptsSelective estrogen receptor modulatorsRegression of endometriosisTreatment of endometriosisEstrogen receptor modulatorsReceptor modulatorsEstrogen-dependent disorderTissue-selective actionSignificant side effectsCD-1 miceEndometrial gene expressionCentral nervous systemEffective novel agentsExpression of PREndometrial stimulationGnRH agonistOvarian enlargementER expressionLIF mRNAExperimental endometriosisEstrogen antagonismER antagonistNovel agentsSERM bazedoxifeneEndometriosisMouse modelEndometrial stem cell transplantation restores dopamine production in a Parkinson’s disease model
Wolff EF, Gao X, Yao KV, Andrews ZB, Du H, Elsworth JD, Taylor HS. Endometrial stem cell transplantation restores dopamine production in a Parkinson’s disease model. Journal Of Cellular And Molecular Medicine 2011, 15: 747-755. PMID: 20406327, PMCID: PMC2998585, DOI: 10.1111/j.1582-4934.2010.01068.x.Peer-Reviewed Original ResearchConceptsParkinson's diseaseDopaminergic neuronsWhole-cell patch-clamp recordingsCell patch-clamp recordingsDopamine metabolite concentrationsPD mouse modelStem cell transplantationDisease modelsSite of lesionParkinson's disease modelPyramidal cell bodiesPatch-clamp recordingsMesenchymal stem-like cellsAllogenic stem cellsStem cellsStem-like cellsCell transplantationStriatal dopamineNeural markers nestinCentral neuronsDopaminergic cellsDendritic projectionsDopamine synthesisDopamine productionMouse modelMaternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming
Martin JR, Lieber SB, McGrath J, Shanabrough M, Horvath TL, Taylor HS. Maternal Ghrelin Deficiency Compromises Reproduction in Female Progeny through Altered Uterine Developmental Programming. Endocrinology 2011, 152: 2060-2066. PMID: 21325042, PMCID: PMC3075930, DOI: 10.1210/en.2010-1485.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsEmbryo ImplantationFemaleFertilityGene Expression Regulation, DevelopmentalGhrelinHeterozygoteHomeobox A10 ProteinsHomeodomain ProteinsImmunohistochemistryLitter SizeMaleMiceMice, KnockoutProliferating Cell Nuclear AntigenReproductionReverse Transcriptase Polymerase Chain ReactionTranscription FactorsUterusWnt ProteinsConceptsGhrelin deficiencyDevelopmental programmingAbnormal endometrial functionFemale wild-type miceUterus of miceLevels of ghrelinRegulation of appetiteWild-type miceReproductive tract developmentWild-type offspringSubsequent subfertilityEndometrial proliferationUnexposed miceEndometrial functionUtero exposureUterine expressionEmbryo implantationOvarian folliclesCorpora luteaGhrelinReproductive tractTract developmentMiceSignificant alterationsSubfertility
2010
Cigarette smoke inhibits recruitment of bone-marrow-derived stem cells to the uterus
Zhou Y, Gan Y, Taylor HS. Cigarette smoke inhibits recruitment of bone-marrow-derived stem cells to the uterus. Reproductive Toxicology 2010, 31: 123-127. PMID: 20955787, PMCID: PMC3207965, DOI: 10.1016/j.reprotox.2010.10.007.Peer-Reviewed Original ResearchConceptsCigarette smoke extractStem cell recruitmentBone marrowCell recruitmentCigarette smokingLong-term organ damageHuman mesenchymal stem cellsStem cellsCigarette smoke exposureEndometrial epithelial cellsDecidualization markers prolactinBone marrow cellsMesenchymal stem cell recruitmentSmoking inhibitsOrgan damageSmoke exposureDecreased incidenceEndometrial cellsFemale infertilitySmoke extractUnfiltered cigarettesFemale C57BL/6JMouse modelCigarette smokeUterine sectionsBisphenol‐A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response
Bromer JG, Zhou Y, Taylor MB, Doherty L, Taylor HS. Bisphenol‐A exposure in utero leads to epigenetic alterations in the developmental programming of uterine estrogen response. The FASEB Journal 2010, 24: 2273-2280. PMID: 20181937, PMCID: PMC3230522, DOI: 10.1096/fj.09-140533.Peer-Reviewed Original ResearchConceptsEpigenetic alterationsCytosine-guanine dinucleotides (CpGs) methylationUtero BPA exposureHomeobox gene HOXA10Developmental programmingDiminished methylationChromatin immunoprecipitationBisulfite sequencingEpigenetic mechanismsDNA methylationPromoter sequencesBPA exposureMethylation profilesExpression patternsGene expressionUterine organogenesisUterine estrogen responsesMethylationNovel mechanismGeneral mechanismPregnant CD-1 miceProtein expressionCD-1 miceHOXA10Expression
2009
Hypermethylation of Homeobox A10 by in Utero Diethylstilbestrol Exposure: An Epigenetic Mechanism for Altered Developmental Programming
Bromer JG, Wu J, Zhou Y, Taylor HS. Hypermethylation of Homeobox A10 by in Utero Diethylstilbestrol Exposure: An Epigenetic Mechanism for Altered Developmental Programming. Endocrinology 2009, 150: 3376-3382. PMID: 19299448, PMCID: PMC2703508, DOI: 10.1210/en.2009-0071.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceDiethylstilbestrolDNA (Cytosine-5-)-MethyltransferasesDNA MethylationEpigenesis, GeneticFemaleGene Expression Regulation, DevelopmentalGenes, HomeoboxHomeobox A10 ProteinsHomeodomain ProteinsHumansMiceMolecular Sequence DataPregnancyPrenatal Exposure Delayed EffectsUterusConceptsDES exposureHOXA10 expressionDevelopmental programmingUtero DES exposureUtero diethylstilbestrol exposureHuman endometrial cellsExpression of HOXA10Homeobox gene HOXA10Female reproductive tractDiethylstilbestrol exposureEndometrial cellsClassical estrogenHomeobox A10Short-term exposureDNA methyltransferases 1Uterine organogenesisDevelopmental anomaliesCaudal portionIncreased expressionHOXA10 geneReproductive tractNonsteroidal estrogensEpigenetic mechanismsExposure resultsDiethylstilbestrol
2008
Experimental Murine Endometriosis Induces DNA Methylation and Altered Gene Expression in Eutopic Endometrium1
Lee B, Du H, Taylor HS. Experimental Murine Endometriosis Induces DNA Methylation and Altered Gene Expression in Eutopic Endometrium1. Biology Of Reproduction 2008, 80: 79-85. PMID: 18799756, PMCID: PMC2804809, DOI: 10.1095/biolreprod.108.070391.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDNA MethylationEndometriosisEndometriumFemaleGene Expression RegulationHomeobox A10 ProteinsHomeodomain ProteinsImmunohistochemistryInsulin-Like Growth Factor Binding Protein 1Integrin beta ChainsKruppel-Like Transcription FactorsMiceReceptors, ProgesteroneReverse Transcriptase Polymerase Chain ReactionRNA, MessengerConceptsEndometriosis groupEndometrial receptivityEutopic endometriumExperimental endometriosisAltered gene expressionInsulin-like growth factorInduction of endometriosisKruppel-like factor 9Expression of HOXA10Total progesterone receptorEndometrial gene expressionBeta3 mRNA expressionProtein-1 mRNAReal-time RT-PCRQuantitative real-time RT-PCRGene expressionMurine endometriosisNormal endometriumProgesterone receptorMethylation-specific PCREndometriosisEndometriumMRNA expressionEctopic locationsGrowth factorHOXA11 is critical for development and maintenance of uterosacral ligaments and deficient in pelvic prolapse
Connell KA, Guess MK, Chen H, Andikyan V, Bercik R, Taylor HS. HOXA11 is critical for development and maintenance of uterosacral ligaments and deficient in pelvic prolapse. Journal Of Clinical Investigation 2008, 118: 1050-1055. PMID: 18274672, PMCID: PMC2242622, DOI: 10.1172/jci34193.Peer-Reviewed Original Research
2007
Contribution of Bone Marrow‐Derived Stem Cells to Endometrium and Endometriosis
Du H, Taylor HS. Contribution of Bone Marrow‐Derived Stem Cells to Endometrium and Endometriosis. Stem Cells 2007, 25: 2082-2086. PMID: 17464086, DOI: 10.1634/stemcells.2006-0828.Peer-Reviewed Original ResearchConceptsBone marrow-derived cellsDonor-derived bone marrow cellsLacZ transgenic miceBone marrow cellsUterine endometriumBone marrowEndometrial cellsPeritoneal cavityTransgenic miceMarrow cellsStem cellsEctopic endometrial implantationNormal endometrial physiologyBone marrow-derived stem cellsBone marrow transplantationMale bone marrowMarrow-derived cellsMarrow-derived stem cellsHuman uterine endometriumEndometrial implantationMesenchymal stem cell originStem cell originMarrow transplantationEndometrial physiologyExperimental endometriosis
2006
Xenoestrogen exposure imprints expression of genes (Hoxa10) required for normal uterine development
Smith CC, Taylor HS. Xenoestrogen exposure imprints expression of genes (Hoxa10) required for normal uterine development. The FASEB Journal 2006, 21: 239-246. PMID: 17093138, DOI: 10.1096/fj.06-6635com.Peer-Reviewed Original ResearchConceptsHOXA10 estrogen response elementEstrogen response elementHOXA10 expressionUterine developmentAbility of BPAReproductive tract alterationsUterine HOXA10 expressionUtero BPA exposureER antagonist ICIExpression of HOXA10Gestational day 9Normal uterine developmentDose-responsive increaseDose-response increaseHOXA10 mRNA expressionHOXA10 antisenseUtero exposureAntagonist ICITract alterationsBPA exposureIshikawa cellsBPA actionEstrogen stimulationEndocrine perturbationsDay 9
2003
Transcriptional Repression of Peri-Implantation EMX2 Expression in Mammalian Reproduction by HOXA10
Troy PJ, Daftary GS, Bagot CN, Taylor HS. Transcriptional Repression of Peri-Implantation EMX2 Expression in Mammalian Reproduction by HOXA10. Molecular And Cellular Biology 2003, 23: 1-13. PMID: 12482956, PMCID: PMC140663, DOI: 10.1128/mcb.23.1.1-13.2003.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBinding SitesCells, CulturedEmbryonic DevelopmentEndometriumEstradiolFemaleHomeobox A10 ProteinsHomeodomain ProteinsHumansMammalsMenstrual CycleMiceMutationOligonucleotides, AntisensePregnancyProgesteroneRecombinant ProteinsRegulatory Sequences, Nucleic AcidRepressor ProteinsReproductionTranscription FactorsTranscription, GeneticConceptsTranscriptional repressionMammalian reproductionNegative transcriptional regulationDivergent homeobox genesPossible evolutionary implicationsSite-directed mutagenesisTransient transfection assaysNegative regulatory relationshipDrosophila orthologUrogenital tract developmentDirection of regulationTranscriptional regulationEvolutionary implicationsGene relationshipsHomeobox genesTranscriptional activationTranscriptional targetsRegulatory regionsEmpty spiraclesRegulatory relationshipsDeletional analysisDNase IEMX2 mRNAConstitutive expressionNorthern analysis