P-516 Defective decidualization secretome in severe preeclampsia

Abstract Study question How defective decidualization (DD) induces a differential secretome compromising embryo invasion in severe preeclampsia (sPE). Summary answer DD endometrial stromal cells isolated from sPE patients secrete response to hormonal stimuli. What is known already Endometrial primary driver of and placentation. This process highly coordinated by estradiol progesterone, which transform the (ESCs) into decidualized specialized secretion specific molecules. The ESCs regulates differentiation decidua, including immune system endothelial function regulation. Previously, we have demonstrated existence vitro vivo women who suffered due an impaired However, molecular mechanism that connects with hostile maternal environment for remains unexplored. design, size, duration Human (n = 3) normal pregnancies as controls were biopsies collected at time late-secretory phase. cultured using established model, three technical replicates per sample condition. Culture media 36) analysed mass spectrometry characterize their global secretome, unveiling secreted factors underlaying sPE. study was 12 months. Participants/materials, setting, methods For decidualization, human days absence or presence stimuli (0.5mM cAMP + 1μM MPA) serum-free media. non-decidualized conditions analyse proteins high-resolution spectrometry-based proteomics. Protein quantification performed MaxQuant Perseus software. approach enables characterization secretory program well discovery proteins. Main results role chance We identified quantified total 1.117 ESCs. In transition status, control group showed significant differences abundance 83 (p-value<0.05), two classical markers (IGFBP1 PRL), other hormonally regulated (e.g. VEGFA, WNT4 MFAP2), supporting validity our experimental method. Then, compared versus patients, altered linked DD. detected 160 significantly deregulated (p-value<0.05) during DD, reported risk LPA TF), modulators MFAP2 TRAP1), mediators maternal-fetal communication (NPTX1) regulators C3, C5, C7, SERPIN). Downregulated associated cytoskeleton organization small GTPase mediated signal transduction, consistent decidualization. contrast, upregulated implicated complement activation, regulation humoral inflammatory response. A heatmap based on successfully classified samples controls, Limitations, reasons caution Sample size six analysing patient (N samples=36) ensure robustness reproducibility. Samples clustering support biological variance higher than variance, effectiveness hallmark identified. Wider implications findings show aberrant These decidual microenvironment might impact invasion, contribution Understanding mechanisms underlying provide new biomarkers prediction. Trial registration number Not applicable