2015
Enhanced Human Decidual Cell–Expressed FKBP51 May Promote Labor-Related Functional Progesterone Withdrawal
Schatz F, Guzeloglu-Kayisli O, Basar M, Buchwalder LF, Ocak N, Guzel E, Guller S, Semerci N, Kayisli UA, Lockwood CJ. Enhanced Human Decidual Cell–Expressed FKBP51 May Promote Labor-Related Functional Progesterone Withdrawal. American Journal Of Pathology 2015, 185: 2402-2411. PMID: 26207680, DOI: 10.1016/j.ajpath.2015.05.014.Peer-Reviewed Original ResearchConceptsTerm decidual cellsDecidual cellsProgesterone receptorP4 withdrawalInterstitial trophoblastMedroxyprogesterone acetateDC culturesHuman term labourLow progesterone receptorsGlucocorticoid receptor expressionFunctional progesterone withdrawalCultured decidual cellsHuman decidual cellsPlasma progesterone levelsThird trimester trophoblastDC nucleiDecidual sectionsOrganon 2058Plasma P4 levelsTerm laborPR expressionProgesterone withdrawalProgesterone levelsReceptor expressionGR expression
2011
Nod1 Activation by Bacterial iE-DAP Induces Maternal–Fetal Inflammation and Preterm Labor
Cardenas I, Mulla MJ, Myrtolli K, Sfakianaki AK, Norwitz ER, Tadesse S, Guller S, Abrahams VM. Nod1 Activation by Bacterial iE-DAP Induces Maternal–Fetal Inflammation and Preterm Labor. The Journal Of Immunology 2011, 187: 980-986. PMID: 21677137, DOI: 10.4049/jimmunol.1100578.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAnimals, NewbornCell LineDiaminopimelic AcidDisease Models, AnimalFemaleHumansInfant, NewbornInfant, PrematureInflammationMaternal-Fetal ExchangeMiceMice, Inbred C57BLNod1 Signaling Adaptor ProteinObstetric Labor, PrematurePregnancyPregnancy OutcomeTissue Culture TechniquesTrophoblastsConceptsPattern recognition receptorsPreterm laborCytokine profileNOD1 activationRecognition receptorsInfection-associated preterm laborHuman first-trimester trophoblastsIntracellular pattern recognition receptorsProinflammatory cytokine profileHuman term placental tissueActivation of NOD1Maternal-fetal interfaceInfection-associated inflammationFunction of NOD1Term placental tissueFirst trimester trophoblastsThird trimester trophoblastFetal inflammationPreterm deliveryEmbryonic day 14.5Pregnancy outcomesFetal weightIL-6MCP-1NOD2 stimulationUric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia
Mulla MJ, Myrtolli K, Potter J, Boeras C, Kavathas PB, Sfakianaki AK, Tadesse S, Norwitz ER, Guller S, Abrahams VM. Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia. American Journal Of Reproductive Immunology 2011, 65: 542-548. PMID: 21352397, PMCID: PMC3114103, DOI: 10.1111/j.1600-0897.2010.00960.x.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsDisease ProgressionEnzyme ActivationFemaleGene Expression Regulation, DevelopmentalHumansHyperuricemiaInflammasomesInterleukin-1betaMaternal-Fetal RelationsNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsPre-EclampsiaPregnancyTrophoblastsUric AcidConceptsIL-1β secretionIL-1β productionMonosodium urateTrophoblast cellsUric acidFirst trimester trophoblast cellsAdverse pregnancy outcomesPathogenesis of preeclampsiaMaternal-fetal interfaceInduction of inflammationActive IL-1βNOD-like receptorsThird trimester trophoblastActive caspase-1Uric acid increasesCaspase-1 activationIL-1β processingPregnancy outcomesInflammatory dysregulationPlacental dysfunctionClinical manifestationsIL-1βInflammasome activationNALP3 inflammasomePreeclampsia
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