Proteomic profile regarding antihypertensive therapy in preeclampsia pregnant
Ontology highlight
ABSTRACT:
INSTRUMENT(S): Q-Exactive (Thermo Fisher)
ORGANISM(S): Homo Sapiens (ncbitaxon:9606)
SUBMITTER: 
Bruna Cavecci Mendonca Valeria Cristina Sandrim Bruno Cesar Rossini Carolina Cristina Pinto Souza Lucilene Delazari dos Santos Julyane Natsumi Saito Kaihara
PROVIDER: MSV000095404 | MassIVE | Mon Jul 22 06:38:00 BST 2024
REPOSITORIES: MassIVE
Similar Datasets
Project description:Preeclampsia (PE) is a common pregnancy disorder, and it complicates 5~7% of all pregnancies. At present, termination of pregnancy is the only curative strategy for PE. To explore a potential target for PE treatment, we collected placental tissue samples from patients with preeclampsia (PE) and normal pregnant women (N), and performed high-throughput RNA sequencing. We found that FOXP2 was significantly downregulated in placental samples of patients with PE compared with the controls.
2024-11-06 | GSE279757 | GEO
Project description:Preeclampsia (PE) is the leading cause of prenatal morbidity and mortality. It is associated with defective trophoblast functions at implantation, but manifestation of its phenotypes is in late pregnancy. There is no reliable method for early prediction and treatment of PE. Adrenomedullin (ADM) is an abundant placental peptide in early pregnancy. Here, integrated single-cell sequencing and spatial transcriptomics confirm a high ADM expression in the human villous cytotrophoblast. The levels of ADM in chorionic villi and serum were lower in first-trimester pregnant women who later developed PE than those with normotensive pregnancy. ADM stimulates differentiation of trophoblast stem cells and trophoblast organoids in vitro. In pregnant mice, placenta-specific ADM suppression led to PE-like phenotypes. The PE-like phenotypes in a mouse PE model were reduced by a novel placenta-specific nanoparticle-based forced expression of ADM. Our study reveals the roles of trophoblastic ADM in placental development, PE pathogenesis and its potential clinical uses.
2023-07-09 | GSE236475 | GEO
Project description:Maternal serum levels of calcyclin and heat shock protein 90 were compared throughout pregnancy from the first trimester till term among women with preeclampsia (PE) and age-matched normotensive pregnant controls (C). Serum samples from two different studies, a nested case-control study embedded in the Rotterdam periconception cohort and the Lepra Study both conducted at the Erasmus MC in Rotterdam. They were collected in the first, second and third trimester of pregnancy in 43 patients with preeclampsia, consisting of 20 early-onset and 23 late-onset preeclampsia, and 46 normotensive pregnant controls. A serum based 2D LC-MS assay on Parallel Reaction Monitoring mode using a high resolution tribrid mass spectrometer was used to quantify both calcyclin and heat shock protein 90.
2018-11-21 | PXD009025 | Pride
Project description:Background: Platelets may be pivotal mediators of the thrombo-haemorrhagic complications of preeclampsia (PE), linking inflammation and thrombosis with endothelial and vascular dysfunction. While gestational hypertension (GH) falls within the spectrum of hypertensive complications of pregnancy and is a risk factor for preeclampsia, it is unclear what biomarkers distinguish PE from GH. Aim: To identify specific plasma and platelet thrombo-inflammatory biomarkers indicative of preeclampsia and distinguish PE from GH. Methods: We performed multiplex immunoassays, assessed platelet and plasma proteomics and metabolomics data of PE patients, and compared with non-pregnant (NP), healthy pregnant (PC) and GH participants. Results: We report plasma proteins upregulated, enriched plasma metabolites and proteins distinctly overexpressed in platelets of PE and GH compared to NP and PC. Whilst procoagulation in PC may be fibrinogen driven, Inter-Alpha-Trypsin Inhibitors ITIH2 and ITIH3 were enriched in hypertensive complications of pregnancy (PE and GH), and fibronectin and S100A8/9 may be major procoagulant agonists in PE but not GH. In addition, platelet leucine-rich repeat-containing protein 27 and 42 (LRRC27/42) subunits of volume-regulated VRAC anion channels were markedly overexpressed in preeclampsia and may contribute to the heightened glucose sensitivity and the pro-thrombotic tendency of this disorder. Additionally, our multiplex immunoassays confirmed previous reports of increases in preeclampsia plasma cytokines, including SDF-1α, which can directly activate platelets; but also, i-309 and CTACK cytokines, whose effects on platelets we explored using STRING analysis. Conclusion: We identified biomarkers that may be monitored for preeclampsia onset and progression, and distinguish PE from GH. Also, through protein-protein interactions analysis, we generated a new hypothesis for platelets’ contribution to the thrombo-inflammatory states of preeclampsia.
2022-03-16 | PXD031278 | Pride
Project description:Preeclampsia (PE) is characterized by sustained hypertension and proteinuria at a gestational age of 20 weeks or more. Immune system alterations are associated with the origin and the pathophysiology of preeclampsia, however, little is known about the landscape and heterogeneity of maternal immune system at the single-cell level. In this study, we performed single-cell RNA sequencing of 80,429 cells in PE patients and health controls, including T cells, B cells, natural killer (NK) cells, myeloid cells in peripheral blood mononuclear cells to characterize the immune cell subgroups at the pregnant and postpartum stages of PE. Our work showed that there was excessive activation of B cells, monocytes and NK cells in PE patients at the pregnant stage. Additionally, lower immune response activation was noticed in CD4+ and CD8+ T cells in PEs, especially the low-activation of memory T cells at the pregnant and postpartum stages. Moreover, there was a higher activation of B cells in pregnancy persisted postpartum in PEs, together with lower activation of memory T cells. These indicated their persistent effects on PE and its recurrence risks.
2022-11-15 | GSE192693 | GEO
Project description:The heart undergoes physiological hypertrophy during pregnancy in healthy individuals. Metabolic syndrome (MetS) is now prevalent in women of child-bearing age and might add risks of adverse cardiovascular events during pregnancy. The present study asks if cardiac remodeling during pregnancy in obese individuals with MetS is abnormal and whether this predisposes them to a higher risk for cardiovascular disorders. The idea that MetS induces pathological cardiac remodeling during pregnancy was studied in a long-term (15 weeks) Western diet–feeding animal model that recapitulated features of human MetS. Pregnant female mice with Western diet (45% kcal fat)–induced MetS were compared with pregnant and nonpregnant females fed a control diet (10% kcal fat). Pregnant mice fed a Western diet had increased heart mass and exhibited key features of pathological hypertrophy, including fibrosis and upregulation of fetal genes associated with pathological hypertrophy. Hearts from pregnant animals with WD-induced MetS had a distinct gene expression profile that could underlie their pathological remodeling. Concurrently, pregnant female mice with MetS showed more severe cardiac hypertrophy and exacerbated cardiac dysfunction when challenged with angiotensin II/phenylephrine infusion after delivery. These results suggest that preexisting MetS could disrupt physiological hypertrophy during pregnancy to produce pathological cardiac remodeling that could predispose the heart to chronic disorders.
2023-07-13 | GSE237063 | GEO
Project description:Preeclampsia (PE) is a multisystem pregnancy complication constituting a major cause of maternal and fetal morbidity and mortality. Factors pointing to a placental origin are the development of the pathology only during pregnancy, and its disappearance in the post-partum period. Our study identified a specific signature of PE including five Gene Ontology clusters including "angiogenesis and differentiation", "cell cycle”, "cell adhesion", "inflammatory response" and "cellular metabolism". Interestingly, we identified DUSP1 as a biomarker of interest in PE. Pregnant women with PE have a higher concentration of DUSP1 in serum in the first trimester of pregnancy compared to healthy donors. Interesting, at a distance from childbirth DUSP1 finds a rate like the control group showing the predictive interest of DUSP1 as a predictive biomarker of PE
2024-03-26 | GSE262147 | GEO
Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia.
2014-05-14 | GSE48424 | GEO
Project description:Preeclampsia (PE) is a major health problem in pregnancy, and miRNAs play a role in the pathophysiology of PE. However, the expression of circulating miRNAs was not analyzed in the second trimester of pregnancy, a period of major relevance to identify predictive biomarkers for PE. Therefore, we examined the expression profiles of 84 circulating miRNAs using PCR-array in plasma collected between 20 and 25 weeks of gestation from pregnant who subsequently developed PE and from those who remained healthy along pregnancy randomly selected from a prospective cohort of pregnant. miR-204-5p (P=0.0082) and other 22 miRNAs were upregulated (fold change > 2.0, while miR-24-3p, miR-22-3p, miR-143-3p, and miR-376c-3p had fold change > 4.0) and six miRNAs were downregulated (fold change < 0.5) in plasma from pregnant who developed PE. Target genes for differentially expressed miRNAs were extracted from the miRTarBase of experimentally validated miRNA-target interactions and used in gene set functional enrichment and REACTOME pathway analysis. The 20 pathways with the lowest false discovery rate for the upregulated and downregulated miRNAs are related to pathophysiology of PE, such as apoptosis, angiogenesis, and signal transduction, including signaling by receptor tyrosine kinases, VEGF and TGFB family members. Moreover, we explored the 37 target genes and pathways for miR-204-5p, including MMP-9, MALAT1, TGFBR2, and SIRT1. The circulating miRNAs differentially expressed in the second trimester of pregnancy are related to target genes and pathways of pathophysiological relevance during the early development of PE, and our findings provide for potential circulating predictive biomarkers in PE. For the PCR array, total RNA isolated was converted into cDNA using the miScript II RT Kit (Qiagen®, Leusden, Netherlands), according to the manufacturer’s instructions
2021-03-15 | GSE168860 | GEO
Project description:Background: Preeclampsia (PE) is a placental disease characterized by hypertension and proteinuria in pregnant women, which is associated with a high maternal and infantile morbidity. However, circulating biomarkers able to predict the prognosis of PE are lacking. Methods: Thirty-eight women were included in the study. They consisted of 19 patients with PE (13 with severe PE and 6 women with non-severe PE) and 19 gestational age-matched normal pregnancy controls. We measured coagulation pathway, endothelial responses and microparticle release and circulating gene expression in PE patient groups and normotensive controls. Results: The measurement of markers associated with coagulation pathway, endothelial activation and circulating microparticles enabled to discriminate PE from normal pregnancy but were not sufficient to distinguish severe from non-severe PE. PE patients also exhibited a specific transcriptional program distinct from that of control women and subtle differences were observed between severe and non-severe PE. Functional annotation of the up-modulated signature in PE highlighted two main functions related to ribosome and complement. Importantly, we found that 8 genes were specifically up-modulated in severe preeclampsia. Among these genes, the expression of VSIG4 was significantly increased in patients with severe preeclampsia in comparison with controls and patients with non-severe preeclampsia. Conclusion: Using transcriptional signatures of blood samples, we identified the gene encoding the estrogen receptor as a potential diagnostic marker of severe preeclampsia. In addition, the determination of this gene may improve the prognostic assessment of severe preeclampsia. Thirty-eight women were included in the study: 19 patients with PE, including 6 women with non-severe PE and 13 with severe PE, and 19 women with normal pregnancy (NP) selected according to age, weight, smoking status, race, gestational age at the inclusion, and blood pH (Table 1 of manuscript). Women with NP had no history of medical illness or medication, and received routing prenatal care. The diagnostic of PE was based on a blood pressure of M-bM-^IM-% 140/90 mmHg taken twice, uricemia above normal laboratory range (120-420 M-BM-5mol/L), and proteinuria higher than 300 mg in a 24 hour-collection, occurring after 20 gestational weeks in previously normotensive women (Table 2). The criteria used to define severe PE included one of the following conditions: a blood pressure higher than 160/110 mmHg, a proteinuria higher than 1500 mg/24h), a multisystem disorder, maternal cerebral symptoms (seizures, stroke) or intrauterine growth restriction below the 3M-BM-0 percentile. Women with multiple gestations, fetal congenital malformations/chromosomal abnormalities, recent infection, antiphospholipid antibodies, trauma, drug or alcohol abuse during pregnancy, preexisting hypertension, thrombophilia with PE history, or women receiving anticoagulant or antiaggregation therapy were excluded from the study. Two microarrays (one non-severe PE and one normal) were discarded from the analysis for technical reasons. Thus, only 36 microarrays are included here.
2014-05-14 | E-GEOD-48424 | biostudies-arrayexpress