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Methods We assessed the deposits of C5b9 complement membrane attack complex on endothelial cells (HMEC-1) that were exposed I in vitro i to cord blood plasma from 13 cases of severe PE and 18 healthy pregnancies (n = 9 preterm and n = 9 term). To evaluate the activation of the complement system in fetuses from pregnancies complicated by severe pre-eclampsia (PE). EP01.30: The complement system is suppressed in fetuses from pregnancies complicated by severe pre-eclampsia. [Extracted from the article]

To evaluate the endothelial dysfunction related to the activation of the complement and coagulation cascade in early-onset severe pre-eclampsia (PE). VP42.11: Influence of activated complement and coagulation cascades on endothelial cell dysfunction in early onset pre-eclampsia Conclusions Complement and coagulation cascades are activated in early-onset severe PE and seem to play an important role in endothelial dysfunction. [Extracted from the article]

To explore the performance of endotheliopathy biomarkers and angiogenic factors in distinguishing pre-eclampsia (PE) from COVID-19 in pregnancy. Conclusions PE could be distinguished from COVID-19 by sFlt1/PlGF ratio and other endotheliopathy biomarkers. VP31.03: Endotheliopathy biomarkers and angiogenic factors in distinguishing pre-eclampsia from COVID-19 in pregnancy. [Extracted from the article]

Results Both COVID-19 and PE induced an overexpression of ICAM-1 and VWF on endothelial cells although the effect of pre-eclampsia was less pronounced than the one triggered by severe COVID-19 (p < 0.05). Conclusions Both COVID-19 and PE trigger endothelial damage and induce the activation of inflammation cell signalling pathways in endothelial cells. To study endothelial damage and alteration in signalling pathways in endothelial cells exposed to sera from pregnant women with PE and COVID-19 I in vitro i . [Extracted from the article]

Conclusions COVID-19 and PE exhibit distinctive profiles of endothelial damage, immune dysregulation and angiogenic imbalance, which could help in the differential diagnosis and development of new therapeutic strategies. Methods Plasma and sera samples were obtained from pregnant women with COVID-19 infection classified into mild (n=10) or severe (n=9) in addition to normotensive pregnancies as controls (n=10) and patients with PE (n=13). To study endothelial damage, microvascular thrombosis, immune response and angiogenic imbalance in pre-eclampsia (PE) and COVID-19 in pregnancy. [Extracted from the article]

Graft-versus-host disease (GVHD) is a complication of allogeneic haematopoietic cell transplantation. Endothelial injury is crucial as pathophysiological substrate for GVHD. GVHD first-line treatment is high-dose corticosteroids, although some patients are steroid-refractory. Through the present study, we compared the endothelial proteomic profiles in response to serum from steroid-refractory acute GVHD (SR-aGVHD) and steroid-sensitive acute GVHD (SS-aGVHD) patients. Blood samples from SR-aGVHD (n = 4) and SS-aGVHD (n = 8) patients were collected at aGVHD diagnosis. Endothelial cell cultures were exposed (48 h) to patients' serum. Protein extraction and proteomic analysis were performed. Differences were statistically evaluated by multivariate analysis. Forty-four proteins contributed to separate all samples into the two study groups, among which 15 participated significantly (p < 0.05), 10 exhibiting a fold change >1.2. Differentially expressed proteins were mainly associated with oxidative phosphorylation (Cytochrome C oxidase subunit 6B1, CX6B1), inflammation and angiogenesis (Apolipoprotein D, APOD), cell survival (Rapamycin-insensitive companion of mTOR, RICTR), and oxidative stress (Riboflavin kinase, RIFK). This pilot study used a novel approach to distinguish the aGVHD response to steroid treatment. The proteins differentially expressed could constitute potential biomarkers for steroid-treatment response. These findings signify a step forward to identify the mechanisms of response to steroids, of high clinical relevance considering the SR-aGVHD elevated mortality., (© 2023 The Authors. Journal of Cellular and Molecular Medicine published by Foundation for Cellular and Molecular Medicine and John Wiley & Sons Ltd.)