2014
In Vivo and In Vitro Evidence for Placental DNA Damage in Preeclampsia
Tadesse S, Kidane D, Guller S, Luo T, Norwitz NG, Arcuri F, Toti P, Norwitz ER. In Vivo and In Vitro Evidence for Placental DNA Damage in Preeclampsia. PLOS ONE 2014, 9: e86791. PMID: 24466242, PMCID: PMC3899334, DOI: 10.1371/journal.pone.0086791.Peer-Reviewed Original ResearchConceptsDecidual stromal cellsCytotrophoblast cellsMaternal decidual stromal cellsReactive oxygen speciesPlacental oxidative stressFetal-maternal interfaceDNA damagePE placental tissuesAnti-oxidant defensesMultisystem diseasePregnant womenPE placentasFetal sideMaternal deciduaOxidative DNA damagePreeclampsiaPlacental tissueNormal placentaStromal cellsPlacentaOxidative stressVitro EvidenceRepair responseDNA damage/repair responseΓH2AX foci
2009
Role of the syncytium in placenta-mediated complications of preeclampsia
Guller S. Role of the syncytium in placenta-mediated complications of preeclampsia. Thrombosis Research 2009, 124: 389-392. PMID: 19535132, PMCID: PMC2764997, DOI: 10.1016/j.thromres.2009.05.016.Peer-Reviewed Original ResearchConceptsPlasminogen activator inhibitor-1Fms-like tyrosine kinase-1Complications of preeclampsiaIntrauterine growth restrictionPathophysiology of preeclampsiaTyrosine kinase-1Immune cell functionAnti-angiogenic factorsActivator inhibitor-1Potential protective actionMaternal hemostasisSoluble endoglinEndothelial functionReperfusion injuryMaternal endotheliumMaternal mortalityRelease of microparticlesGrowth restrictionMaternal bloodPreeclampsiaSensitive markerMajor causeInhibitor-1Protective actionReactive oxygen species
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
2006
Differential Release of Plasminogen Activator Inhibitors (PAIs) During Dual Perfusion of Human Placenta: Implications in Preeclampsia
Guller S, Ma Y, Malek A, Di Santo S, Schneider H. Differential Release of Plasminogen Activator Inhibitors (PAIs) During Dual Perfusion of Human Placenta: Implications in Preeclampsia. Placenta 2006, 28: 278-285. PMID: 16820203, DOI: 10.1016/j.placenta.2006.05.005.Peer-Reviewed Original ResearchConceptsIntrauterine growth restrictionPAI-1 levelsPlasminogen activator inhibitorTotal PAI-1 levelsMaternal perfusateDual perfusionTime-dependent increaseReactive oxygen speciesRelease of PAIActivator inhibitorIntervillous fibrin depositionActive PAI-1 levelsSignificant time-dependent increasePAI-2 levelsPAI-1 releaseHuman term placentaPlacental tissue extractsAberrant fibrinolysisPlacental infarctionMaternal serumFibrin depositionGrowth restrictionIntervillous spacePreeclampsiaTerm placenta