Scutellariae Radix and Atractylodis Macrocephalae Rhizoma pairs ameliorate preeclampsia via PI3K/AKT/eNOS pathway
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus Musculus
SUBMITTER: 
Yong Liu
PROVIDER: PXD063136 | iProX | Fri Apr 18 00:00:00 BST 2025
REPOSITORIES: iProX
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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: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 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: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
Project description:Preeclampsia is one of the most common pregnancy disorders, and characterized by insufficient trophoblast invasion and placental inflammation. RNA sequencing was performed using placental tissues collected from PE patients and control healthy pregnant women. The results showed that OTU deubiquitinase, ubiquitin aldehyde binding 2 (OTUB2) was downregulated in placenta from PE patients.
2025-08-20 | GSE303543 | GEO
Project description:Preeclampsia (PE) is a hypertensive pregnancy syndrome associated with target organ damage and higher cardiovascular sequelae and requires antihypertensive therapy. However, about 40% of patients are nonresponsive to treatment, leading to worse clinical outcomes. Through proteomics, we aimed to compare the circulating protein profiles and identify differentially expressed proteins of 10 responsive (R-PE) and 10 nonresponsive (NR-PE) patients to 10 healthy pregnant controls (HP). We performed plasma protein relative quantification using mass spectrometry.
2024-07-22 | MSV000095404 | MassIVE
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:Defective deep placentation, an abnormal transformation of the spiral arteries in the junctional zone of the myometrium, is known to cause significant obstetrical complications such as preeclampsia (PE), fetal growth restriction, and placental infarcts with fetal death. Serological biomarkers to predict and diagnose PE would help antenatal care and reduce the obstetrical complications. To discover biomarkers for prediction of PE, we first performed global proteome profiling of three pairs of maternal plasma samples obtained from the early second trimester pregnant women who subsequently developed PE and controls to identify proteins that were abundant in the patients. We further evaluated the expression changes of PE representing proteins in stored plasma samples of a cohort of subsequently developed PE and their matched controls by MRM assay. We identified both Complement C1s subcomponent (p-value = 0.041) and Protein AMBP (p-value = 0.043) were up-regulated in the cohort of PE plasma samples before manifestation of clinical disease. We propose that these proteins may be involved in the remodeling process of the spiral arteries even before the manifestation of PE. These proteins could be served as potential plasma biomarkers to predict pregnant women at increased risk of developing PE.
2018-07-05 | PXD003419 | Pride
Project description:Preeclampsia (PE), affecting 2-8% of all pregnancies, is a multiorgan disease and characterized by elevated blood pressure and proteinuria after 20 weeks of gestation. It is a major cause of maternal and perinatal morbidity and mortality worldwide. there are benefits for early intervention however sensitive early deetection biomarkers are not available. With label-free quantitative proteomics we quantified urine proteins in 17 pregnant women sampled at every trimester. three hudnred sixy one proteins were quantified with 2 or more unique peptides and several proteins could classify the preecalmpsia vs healthy vs women at risk.
2022-08-03 | PXD010276 | Pride
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