2017
Low molecular weight heparin and aspirin exacerbate human endometrial endothelial cell responses to antiphospholipid antibodies
Quao ZC, Tong M, Bryce E, Guller S, Chamley LW, Abrahams VM. Low molecular weight heparin and aspirin exacerbate human endometrial endothelial cell responses to antiphospholipid antibodies. American Journal Of Reproductive Immunology 2017, 79 PMID: 29135051, PMCID: PMC5728699, DOI: 10.1111/aji.12785.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, AntiphospholipidAntiphospholipid SyndromeAspirinBeta 2-Glycoprotein ICells, CulturedChemokinesDisease ProgressionDrug Therapy, CombinationEndometriumEndothelial CellsFemaleHeparin, Low-Molecular-WeightHumansMembrane ProteinsNeovascularization, PhysiologicPregnancyPregnancy ComplicationsTrophoblastsVascular Endothelial Growth Factor AVascular Endothelial Growth Factor Receptor-1ConceptsLow molecular weight heparinHuman endometrial endothelial cellsMolecular weight heparinUterine endotheliumAntiphospholipid antibodiesWeight heparinInfluence of LMWHLow dose low molecular weight heparinAnti-angiogenic sFlt-1Chemokine MCP-1Endometrial endothelial cellsEffects of aPLSFlt-1 releaseAngiogenic factor secretionObstetric APSPregnancy complicationsControl IgGChemokine profilesEndothelium dysfunctionChemokine secretionPro-angiogenic VEGFCombination therapySFlt-1Impaired placentationMCP-1
2016
Inflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE)
Shaw J, Tang Z, Schneider H, Saljé K, Hansson SR, Guller S. Inflammatory processes are specifically enhanced in endothelial cells by placental-derived TNF-α: Implications in preeclampsia (PE). Placenta 2016, 43: 1-8. PMID: 27324092, DOI: 10.1016/j.placenta.2016.04.015.Peer-Reviewed Original ResearchConceptsPro-inflammatory cytokine secretionMaternal perfusateCytokine secretionEndothelial dysfunctionActivation markersEndothelial cellsTNF-α blocking antibodyDual perfusion modelMaternal endothelial dysfunctionPro-inflammatory cytokinesMCP-1 secretionTNF-α actionEndothelial cell linePlacental pathophysiologyEndothelial activationIL-6IL-8Maternal endotheliumInflammatory processDual perfusionMaternal circulationBlocking antibodiesPreeclampsiaTNFPerfusion model
2012
Lipopolysaccharide Appears to Activate Human Endometrial Endothelial Cells Through TLR‐4‐Dependent and TLR‐4‐Independent Mechanisms
Krikun G, Trezza J, Shaw J, Rahman M, Guller S, Abrahams VM, Lockwood CJ. Lipopolysaccharide Appears to Activate Human Endometrial Endothelial Cells Through TLR‐4‐Dependent and TLR‐4‐Independent Mechanisms. American Journal Of Reproductive Immunology 2012, 68: 233-237. PMID: 22672000, PMCID: PMC3418410, DOI: 10.1111/j.1600-0897.2012.01164.x.Peer-Reviewed Original ResearchConceptsEndometrial endothelial cellsTissue factor expressionHuman endometrial endothelial cellsToll-like receptorsLPS-RSFactor expressionEndothelial cellsBacterial lipopolysaccharideTLR-4Innate immunityCytokine/chemokine responsesTLR-4 antagonistGram-negative bacterial lipopolysaccharideChemokine responsesIL-6IL-8Cytokine secretionG-CSFWestern blotLipopolysaccharideBacterial componentsCell-free supernatantMD-2ImmunitySecretion
2007
Expression of Toll-like receptors in the human decidua.
Krikun G, Lockwood CJ, Abrahams VM, Mor G, Paidas M, Guller S. Expression of Toll-like receptors in the human decidua. Histology And Histopathology 2007, 22: 847-54. PMID: 17503341, DOI: 10.14670/hh-22.847.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Vesicular TransportCells, CulturedDeciduaEndometriumEndothelial CellsFemaleHumansImmunity, InnateImmunohistochemistryInterleukinsLipopolysaccharidesMyeloid Differentiation Factor 88NF-kappa BPeptidoglycanPoly I-CPregnancyPregnancy Trimester, FirstPregnancy Trimester, ThirdReverse Transcriptase Polymerase Chain ReactionRNA, MessengerSignal TransductionToll-Like ReceptorsConceptsToll-like receptorsHuman deciduaFirst trimester elective terminationMaternal spiral arteriesInnate immune responseCesarean sectionSpiral arteriesThird trimesterCytokine productionElective terminationDecidual tissuesImmune responseLate gestationPregnant endometriumFetal membranesSurveillance moleculeHost defensePregnancyDeciduaMRNA levelsReceptorsMicrobial pathogensTrimesterEndometriumArtery
2004
Differential Effects of Lipopolysaccharide and Thrombin on Interleukin‐8 Expression in Syncytiotrophoblasts and Endothelial Cells: Implications for Fetal Survival
MA Y, KADNER SS, GULLER S. Differential Effects of Lipopolysaccharide and Thrombin on Interleukin‐8 Expression in Syncytiotrophoblasts and Endothelial Cells: Implications for Fetal Survival. Annals Of The New York Academy Of Sciences 2004, 1034: 236-244. PMID: 15731315, DOI: 10.1196/annals.1335.025.Peer-Reviewed Original ResearchConceptsCytokine expressionEndothelial cellsFetal survivalInfection-associated changesPlacental cytokine expressionTissue factor-initiated blood coagulationIL-8 levelsInterleukin-8 levelsAnti-inflammatory steroidsMaintenance of pregnancyIL-8 expressionIL-8 mRNAInterleukin-8 expressionEffect of thrombinHuman umbilical vein endothelial cellsHuman term placentaUmbilical vein endothelial cellsVein endothelial cellsCytokine responsesCytokine productionProinflammatory processesIL-8Inflammatory responseLPS treatmentIntervillous space