2024
TET3-overexpressing macrophages promote endometriosis
Lv H, Liu B, Dai Y, Li F, Bellone S, Zhou Y, Mamillapalli R, Zhao D, Venkatachalapathy M, Hu Y, Carmichael G, Li D, Taylor H, Huang Y. TET3-overexpressing macrophages promote endometriosis. Journal Of Clinical Investigation 2024, 134: e181839. PMID: 39141428, PMCID: PMC11527447, DOI: 10.1172/jci181839.Peer-Reviewed Original ResearchDisease-associated macrophagesTET3 overexpressionHuman endometriosis lesionsPathophysiology of endometriosisPro-inflammatory cytokine productionChronic inflammatory diseaseReproductive age womenEndometriosis lesionsE3 ubiquitin ligasePathogenic macrophagesCytokine productionEndometriosisInflammatory diseasesTET3 knockdownEndometriosis progressionPathogenic contributorsLet-7 miRNA expressionAge womenMacrophagesMouse macrophagesTherapeutic targetUbiquitin ligaseTET3MiceDisease
2021
Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression
Kotlyar AM, Mamillapalli R, Flores VA, Taylor HS. Tofacitinib alters STAT3 signaling and leads to endometriosis lesion regression. Molecular Human Reproduction 2021, 27: gaab016. PMID: 33693775, PMCID: PMC8454207, DOI: 10.1093/molehr/gaab016.Peer-Reviewed Original ResearchConceptsLesion regressionIshikawa cellsJAK/STATGrowth factor mRNA levelsEffects of tofacitinibTreatment of endometriosisHypoxia-inducible factor-1αVascular endothelial growth factor (VEGF) mRNA levelsFactor mRNA levelsWidespread clinical useWestern blot analysisVehicle treatmentOral gavageGynecologic conditionsC57BL/6 miceEutopic endometriumJanus kinase/signal transducerReproductive ageEndometriosisJAK inhibitorsKinase/signal transducerTofacitinibTherapeutic targetLesion growthClinical use
2020
Hepatic TET3 contributes to type-2 diabetes by inducing the HNF4α fetal isoform
Da Li, Cao T, Sun X, Jin S, Di Xie, Huang X, Yang X, Carmichael GG, Taylor HS, Diano S, Huang Y. Hepatic TET3 contributes to type-2 diabetes by inducing the HNF4α fetal isoform. Nature Communications 2020, 11: 342. PMID: 31953394, PMCID: PMC6969024, DOI: 10.1038/s41467-019-14185-z.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsDiabetes Mellitus, Type 2DioxygenasesDisease Models, AnimalDNA DemethylationDNA MethylationDNA-Binding ProteinsFastingGene Expression RegulationGlucagonGlucoseHepatocyte Nuclear Factor 3-betaHepatocyte Nuclear Factor 4LiverMaleMiceMice, Inbred C57BLMice, KnockoutPromoter Regions, GeneticProtein IsoformsTranscriptional ActivationTranscriptomeUp-RegulationConceptsHepatic glucose productionType 2 diabetesGlucose homeostasisAdult liverSystemic glucose homeostasisPotential therapeutic targetGenetic mouse modelsFetal versionKey gluconeogenic genesMouse modelTherapeutic targetHNF4α functionGlucose productionFetal isoformsLiverT2D.DiabetesPromoter demethylationGluconeogenic genesTET3 overexpressionHNF4αHomeostasisTET3Regulatory mechanismsIsoforms
2019
Potential roles of aquaporin 9 in the pathogenesis of endometriosis
Choi YS, Park JH, Yoon JK, Yoon JS, Kim JS, Lee JH, Yun BH, Park JH, Seo SK, Cho S, Lee BS, Taylor HS. Potential roles of aquaporin 9 in the pathogenesis of endometriosis. Molecular Human Reproduction 2019, 25: 373-384. PMID: 31070762, DOI: 10.1093/molehr/gaz025.Peer-Reviewed Original ResearchConceptsHuman endometrial stromal cellsPathogenesis of endometriosisEndometrial stromal cellsPotential therapeutic targetExpression of MMP2P38 MAPK proteinWestern blot analysisControl patientsEndometrial expressionPhosphorylated ERK 1/2Ectopic endometriumEutopic endometriumInflammatory processLaparoscopic surgeryEndometriosisTherapeutic targetBenign conditionsAQP subtypesExpression of AQP9Stromal cellsTumor developmentWestern blottingAQP9 expressionHealing assaysERK 1/2
2013
Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology.
Bruner-Tran KL, Herington JL, Duleba AJ, Taylor HS, Osteen KG. Medical management of endometriosis: emerging evidence linking inflammation to disease pathophysiology. Minerva Obstetrics And Gynecology 2013, 65: 199-213. PMID: 23598784, PMCID: PMC3718308.Peer-Reviewed Original ResearchConceptsPeritoneal microenvironmentMedical managementDisease pathophysiologyEndometrial progesterone resistanceAppropriate medical managementPathogenesis of endometriosisProgesterone-responsive genesNew therapeutic targetsDisease developmentFemale reproductive tractProgesterone resistanceProinflammatory processesEutopic endometriumRisk factorsProgesterone actionPatients exhibitTherapeutic targetEndometriosisReproductive tractProtein expressionNovel mechanistic frameworkEndometriumInflammationPathophysiologyDisease establishment
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