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
2008
Placental expression of ceruloplasmin in pregnancies complicated by severe preeclampsia
Guller S, Buhimschi CS, Y Y, Huang T, Yang L, Kuczynski E, Zambrano E, Lockwood CJ, Buhimschi IA. Placental expression of ceruloplasmin in pregnancies complicated by severe preeclampsia. Laboratory Investigation 2008, 88: 1057-1067. PMID: 18679377, PMCID: PMC2682720, DOI: 10.1038/labinvest.2008.74.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Severe preeclampsiaReperfusion injurySFlt-1Soluble fms-like tyrosine kinase-1Fms-like tyrosine kinase-1Ischemia/reperfusion injuryLife-threatening syndromeSubsequent reperfusion injuryTerm control groupPathophysiology of preeclampsiaTyrosine kinase-1Activator inhibitor-1Release of factorsSignificant increasePresence of mRNAUpregulation of mRNACeruloplasmin mRNAPlacental damagePlacental factorsMicroarray gene profilingEndothelium dysfunctionPE placentasQuantitative real-time PCRIntervillous spaceThe 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