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
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