2011
Maternal 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
HOXA11 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
Differential Cell-Specific Modulation of HOXA10 by Estrogen and Specificity Protein 1 Response Elements
Martin R, Taylor MB, Krikun G, Lockwood C, Akbas GE, Taylor HS. Differential Cell-Specific Modulation of HOXA10 by Estrogen and Specificity Protein 1 Response Elements. The Journal Of Clinical Endocrinology & Metabolism 2007, 92: 1920-1926. PMID: 17311863, DOI: 10.1210/jc.2006-1694.Peer-Reviewed Original ResearchMeSH KeywordsBreastCells, CulturedElectrophoretic Mobility Shift AssayEstrogensFemaleGenes, ReporterHomeobox A10 ProteinsHomeodomain ProteinsHumansImmunohistochemistryLuciferasesPlasmidsReceptors, EstrogenResponse ElementsReverse Transcriptase Polymerase Chain ReactionSp1 Transcription FactorTransfectionUterusConceptsEstrogen response elementHOXA10 estrogen response elementResponse elementSp1 sitesShift assaysStage-specific expression patternsTissue specificityElectrophoretic mobility shift assaysCell typesSpecificity protein 1Mobility shift assaysAdult reproductive tractGel shift assaysDifferential cellular expressionDistinct differential expressionHox genesSp1 proteinCell-specific modulationTranscription factorsEmbryonic developmentRegulatory elementsExpression patternsReporter assaysBreast MCF-7 cellsDifferential expression
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