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In the ex\u00a0vivo approach, soluble tumor necrosis factor\u2010a receptor 1 (sTNFR1), vascular cell adhesion molecule\u20101 (sVCAM\u20101), intercellular adhesion molecule\u20101 (sICAM\u20101), Von Willebrand factor (sVWF), terminal complement complex (sC5b\u20109), Factor H, complement component C3a and Factor Bb were analyzed in fetal cord blood samples. In the in\u00a0vitro model, vascular cell adhesion molecule\u20101 (VCAM\u20101), intercellular adhesion molecule\u20101 (ICAM\u20101), Von Willebrand factor (VWF), vascular endothelial cadherin (VE\u2010Cadherin), endothelial nitric oxide synthase (eNOS), reactive oxygen species (ROS) and C5b\u20109 deposits were evaluated on endothelial cells in culture exposed to fetal sera or plasma.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Increased sVCAM\u20101, sICAM\u2010 l and decreased Factor H and Factor Bb concentrations were detected in preeclampsia fetuses as compared to fetuses from normotensive mothers (509.4\u2009\u00b1\u200928 vs. 378.4\u2009\u00b1\u200934.3\u2009ng\/mL, 161.1\u2009\u00b1\u200911.9 vs. 114.8\u2009\u00b1\u20096.8, 199.6\u2009\u00b1\u200918.3 vs. 267.1\u2009\u00b1\u200915.4\u2009ng\/mL and 6.6\u2009\u00b1\u20090.7 vs. 10.3\u2009\u00b1\u20091.4 \u03bcg\/mL respectively, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05) with similar results in sTNFR1, sVWF, sC5b\u20109 and C3a. Endothelial cells exposed to fetal sera from preeclampsia showed incremented expression of VCAM\u20101(38.1\u2009\u00b1\u20091.4% vs. 28.3\u2009\u00b1\u20091.6%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01), ICAM\u20101 (12\u2009\u00b1\u20090.9% vs. 8.6\u2009\u00b1\u20090.6%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), VWF (43.5\u2009\u00b1\u20092.9% vs. 3.7\u2009\u00b1\u20090.3%, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.05), and ROS (5\u2009\u00d7\u200910<jats:sup>13<\/jats:sup>\u2009\u00b1\u20091\u2009\u00d7\u200910<jats:sup>12<\/jats:sup> vs. 3.5\u2009\u00d7\u200910<jats:sup>13<\/jats:sup>\u2009\u00b1\u20091.4\u2009\u00d7\u200910<jats:sup>12<\/jats:sup>, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01) with similar expression of VE\u2010Cadherin and eNOS as compared to those exposed to control fetuses. While soluble C5b\u20109 was similar between the study groups (851.4\u2009\u00b1\u2009177.5 vs. 751.4\u2009\u00b1\u2009132.81\u2009ng\/mL, <jats:italic>p<\/jats:italic>\u2009&gt;\u20090.05), significantly less C5b\u20109 deposits on endothelial cells were induced by fetal plasma from preeclamptic compared to normotensive mothers (fold change 0.08\u2009\u00b1\u20090.02 vs. 0.48\u2009\u00b1\u20090.13, <jats:italic>p<\/jats:italic>\u2009&lt;\u20090.01).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>High levels of endothelial adhesion molecules and oxidative stress products suggest endothelial damage and reduced in\u00a0vitro deposition of C5b\u20109 indicates complement dysregulation in preeclampsia fetuses. More research is necessary to study the impact of preeclampsia on fetal vascular health and innate immunity.<\/jats:p><\/jats:sec>","DOI":"10.1111\/aogs.15072","type":"journal-article","created":{"date-parts":[[2025,3,11]],"date-time":"2025-03-11T13:10:29Z","timestamp":1741698629000},"page":"829-838","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":6,"title":["Endothelial damage and complement dysregulation in fetuses from pregnancies complicated by preeclampsia"],"prefix":"10.1111","volume":"104","author":[{"given":"Alex","family":"Ramos","sequence":"first","affiliation":[{"name":"Hemostasis and Erythropathology Laboratory, Hematopathology, Department of Pathology, Centre de Diagn\u00f2stic Biom\u00e8dic (CDB), Hospital Cl\u00ednic de Barcelona, Institut d'Investigacions Biom\u00e8diques August Pi i Sunyer (IDIBAPS) Universitat de Barcelona  Barcelona Spain"},{"name":"Barcelona Endothelium Team  Barcelona 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