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
2010
Protein composition of microparticles shed from human placenta during placental perfusion: Potential role in angiogenesis and fibrinolysis in preeclampsia
Guller S, Tang Z, Ma YY, Di Santo S, Sager R, Schneider H. Protein composition of microparticles shed from human placenta during placental perfusion: Potential role in angiogenesis and fibrinolysis in preeclampsia. Placenta 2010, 32: 63-69. PMID: 21074265, PMCID: PMC3762591, DOI: 10.1016/j.placenta.2010.10.011.Peer-Reviewed Original ResearchMeSH KeywordsCell-Derived MicroparticlesCells, CulturedFemaleFibrinolysisHumansMolecular WeightNeovascularization, PhysiologicPerfusionPlacentaPre-EclampsiaPregnancyProteinsProteomeConceptsPlasminogen activator inhibitorMaternal perfusateSFlt-1Maternal endothelial cell dysfunctionFms-like tyrosine kinasePathophysiology of preeclampsiaMaternal-fetal interfaceEndothelial cell dysfunctionAnti-angiogenic actionFollowing relative levelsPlacental damagePlacental perfusionMaternal serumNormal pregnancyPlacental pathophysiologyAnnexin V bindingSyncytiotrophoblast microparticlesDual perfusionAngiogenic balanceCell dysfunctionMaternal bloodPreeclampsiaActivator inhibitorCytometric analysisLevel of expression
2008
The Placental Syncytium and the Pathophysiology of Preeclampsia and Intrauterine Growth Restriction
Guller S, Y. Y, Fu H, Krikun G, Abrahams VM, Mor G. The Placental Syncytium and the Pathophysiology of Preeclampsia and Intrauterine Growth Restriction. Annals Of The New York Academy Of Sciences 2008, 1127: 129-133. PMID: 18443340, PMCID: PMC3671376, DOI: 10.1196/annals.1434.015.Peer-Reviewed Original ResearchConceptsIntrauterine growth restrictionPathophysiology of preeclampsiaGrowth restrictionPlacental syncytiumFms-like tyrosine kinase-1Complications of pregnancyPlasminogen activator inhibitor-1Tyrosine kinase-1Activator inhibitor-1Release of factorsPlacental damageSoluble endoglinEndothelium dysfunctionLaser capture microdissectionMaternal bloodAntiangiogenic factorsPreeclampsiaFas ligandWestern blottingInhibitor-1Reactive oxygen speciesCapture microdissectionPregnancyPathophysiologyKinase 1