Placental 4D Label-free quantitative proteome and malonylation quantitative modificomics analysis
Ontology highlight
ABSTRACT:
INSTRUMENT(S):
ORGANISM(S): Homo Sapiens (human)
TISSUE(S): Placenta
SUBMITTER: 
Yaling Feng
LAB HEAD: Yaling Feng
PROVIDER: PXD075276 | Pride | 2026-07-01
REPOSITORIES: Pride
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Project description:As one of the most common maternal comorbidities, gestational diabetes mellitus (GDM) and preeclampsia (PE) are associated with maternal and infant health. Although the pathogenesis of PE and GDM remains controversial, oxidative stress is thought to be involved in the underlying pathology of GDM and PE. Protein lysine acetylation (Kac) plays an important regulatory role in biological processes. There is little data regarding the association of the maternal acetylome with GDM and PE. This study aimed to assess the multi-omics (proteome and acetylome) potential value in the underlying pathology for GDM and PE by label-free quantification proteomics technology. In our study, we included placental tissue from healthy individuals (n=6), GDM patients (n=6), and PE patients (n=6). We identified 22 overlapping DEPs (differentially expressed proteins) and 192 overlapping DAPs (differentially acetylated proteins) between the GDM and PE groups. Furthermore, 192 overlapping DAPs were mainly enriched in endoplasmic reticulum stress and ferroptosis pathways. Interestingly, endoplasmic reticulum stress, ferroptosis, and oxidative stress are believed to be related to each other. We also identified that acetylation of the HSP90AA1, HSPA8, PDIA3, GPX4, TF, and CP might serve as novel markers and better therapeutic targets in both complications. We thoroughly analyzed the key characteristics of proteome and acetylome in GDM and PE placental tissues, which may be useful for exploring the underlying pathology and discovering new biomarkers and therapeutic targets.
2024-01-25 | PXD032981 | Pride
Project description:During human pregnancy, a subset of placental cytotrophoblasts (CTBs) differentiates into cells that aggressively invade the uterus and its vasculature, anchoring the progeny and rerouting maternal blood to the placenta. In preeclampsia (PE), CTB invasion is limited, reducing placental perfusion and/or creating intermittent flow. This syndrome, affecting 4-8% of pregnancies, entails maternal vascular alterations (e.g., high blood pressure, proteinuria, and edema) ± fetal growth restriction. The only cure is removal of the faulty placenta, i.e., delivery. Previously we showed that defective CTB differentiation contributes to the placental component of PE, but the causes were unknown. Here, CTBs isolated from PE and control placentas were cultured for 48 h, enabling differentiation/invasion. In various severe forms of PE, transcriptomics revealed common aberrations in CTB gene expression immediately after isolation that resolved in culture. The upregulated genes included SEMA3B. Adding this protein to normal CTBs inhibited invasion and re-created aspects of the phenotype of these cells in PE. Additionally, SEMA3B downregulated VEGF signaling through the PI3K/AKT and GSK3 pathways, effects that were observed in PE CTBs. We propose that, in severe PE, the in vivo environment dysregulates CTB gene expression, the autocrine actions of the upregulated molecules, including SEMA3B, impair differentiation/invasion/signaling and patient-specific factors determine the signs.
2012-08-17 | GSE40182 | GEO
Project description:Preeclampsia (PE) has been associated with placental dysfunction, resulting in foetal hypoxia, accelerated erythropoiesis and increased erythroblast count in the umbilical cord blood (UCB). Although the detailed effects remain unknown, placental dysfunction can also cause inflammation, nutritional and oxidative stress in the fetus that can affect erythropoiesis. Here, we compared the expression of surface adhesion molecules and erythroid differentiation capacity of UCB hematopoietic stem/ progenitor cells (HSPCs), UCB erythroid profiles along with transcriptome and proteome of these cells between male and female foetuses from PE and normotensive pregnancies. While no significant differences were observed in UCB HSPC migration/ homing and in vitro erythroid colony differentiation, the UCB HSPC transcriptome and the proteomic profile of the in vitro differentiated erythroid cells differed between PE vs normotensive samples. Accordingly, despite absence of significant differences in the UCB erythroid populations in male or female foetuses from PE or normotensive pregnancies, transcriptional changes were observed during erythropoiesis, particularly affecting male foetuses. Pathway analysis suggested deregulation in mTORC1/AMPK signaling pathways controlling cell cycle, differentiation and protein synthesis. These results associate PE with transcriptional and proteomic changes in foetal HSPCs and erythroid cells that may underlie the higher erythroblast count in the UCB in PE.
2019-06-20 | PXD010364 | Pride
Project description:Preeclampsia (PE), a hypertensive disorder in pregnancy, is linked to placental vascular remodelling, increasing risks of fetal growth restriction and long-term offspring health problems. The role of fetoplacental endothelial cell-derived extracellular vesicles (EVs) in PE remains underexplored. This study investigates whether EV composition in PE is altered, potentially contributing to impaired fetal development. Small EVs (sEVs) were isolated from primary fetoplacental endothelial cells (fpECs) of term (T), preterm (PT), and early-onset PE (EO-PE) pregnancies. sEVs were characterized using transmission electron microscopy, nanoparticle tracking analysis, and Western blotting, confirming spherical morphology, size (<200nm), and expression of canonical EV and endothelial markers. Proteomic profiling via nano-LC MS/MS and gene set enrichment analysis revealed consistent proteomes in fpEC-derived sEVs, but EO-PE-derived sEVs showed heterogeneity and functional alterations compared to T- and PT-derived sEVs. Notably, EO-PE sEVs were enriched in proteins linked to epithelial-to-mesenchymal transition and myogenesis, processes tied to tissue remodelling and vascular homeostasis, all hallmarks in PE. This signature may transmit signals of endothelial dysfunction to the fetus. In contrast, T-sEVs were enriched in cell cycle and DNA repair pathways. These findings underscore the role of fetoplacental-derived EVs in placental-fetal communication under pathophysiological conditions.
2026-03-09 | PXD068733 | Pride
Project description:An important question for the use of the mouse as a model for studying human disease is the degree of functional conservation of genetic control pathways from human to mouse. The human and mouse placenta show structural similarities but there have been no systematic attempt to assess their molecular similarities or differences. We built a comprehensive database of protein and microarray data for the highly vascular exchange region micro-dissected from the human and mouse placenta near-term. Abnormalities in this region are associated with two of the most common and serious complications of human pregnancy, maternal preeclampsia (PE) and fetal intrauterine growth restriction (IUGR), each disorder affecting ~5% of all pregnancies. Over 7,000 orthologs were detected with 70% co-expressed and over 80% of genes known to cause placental phenotypes in mouse were co-expressed. These genes form a tight protein-protein interaction network with novel candidate genes likely to be important in placental structure and/or function. The entire data is available as a web-accessible database to guide the informed development of mouse models to study human disease This experiment is now fully represented in NCBI Peptidome database with accession PSE115; http://www.ncbi.nlm.nih.gov/peptidome/search/index.shtml?acc=PSE115 Microdissection of human villous trees and mouse placental labyrinth. Tissues were split for microarray and protein analysis. For protein analysis samples were first fractionated by differential sucrose gradients into mitochrondria, cytosol, microsomes and nuclei. Mitochrondira and neuclei were each extracted by two different methods for soluble and insoluble material. Each subcellular fraction for each tissue was analysed in quintuplet by 9 step 2 dimensional LC/MSMS. This generated a total of 270 mzXML files for each tissue.
2009-06-29 | E-GEOD-13299 | biostudies-arrayexpress
Project description:Background: The placenta is known to be critical in the etiology of preeclampsia (PE). However, there is a subset of PE cases without identifiable placental pathology. We evaluated which clinical PE classification system best distinguishes PE with placental pathology from PE without placental pathology. Methods: We evaluated five placental pathologic features in 197 placentas from PE patients grouped by three clinical PE subclasses. 1. PE with calculated infant birthweight <10th percentile (small) for gestational age (SGA PE) versus PE with birthweight ≥10th percentile for gestational age (NSGA PE). 2. PE with delivery before 34 weeks of gestation (EDPE) versus PE with delivery at or after 34 weeks of gestation (LDPE) and 3. PE with severe features versus PE without severe features. Clinical, histologic and molecular findings in patients with PE were compared to normotensive patients, with and without SGA infants (N = 1,078 total). Results: The SGA versus NSGA PE classification system performed best (likelihood ratios (95% CI) for ≥ 3 of 5 placenta pathologic findings: 15.7 (6.5, 38.1) in SGA PE vs. NSGA PE; 6.8 (4.3, 10.8) in EDPE vs. LDPE and 5.2 (1.95, 14.1) in PE with SF vs. PE without SF; all p <.0001). SGA PE and SGA normotensive placentas were abnormal and shared alterations in hypoxia, TNF alpha, glycolysis, unfolded protein response, estrogen response, UV response, p53, TGF beta and mTORC1 signaling pathways. Conclusions: Classifying PE based on birthweight percentile for gestational age is the most useful system for consistently identifying PE associated with placenta pathology.
2026-01-14 | GSE310940 | GEO
Project description:The aim of the study was to compare gene expression profiles in decidua basalis from cases with complicated pregnancies to those from healthy pregnant controls. Cases included pregnant women with preeclampsia (PE) and/or fetal growth restriction (FGR). Decidual tissue was obtained by vacuum suction of the placental bed after the placenta was delivered. Women with PE and/or FGR were included as cases. PE was defined as persistent hypertension (blood pressure (BP) ¡Ý 140/90 mm Hg), plus proteinuria (¡Ý0.3g/24 h or ¡Ý2+ according to a dipstick test), developing after 20 weeks of pregnancy. FGR implied birth weight under 2 standard deviations (SD) below the expected birth weight, as related to gestational age (GA) and sex. Due to tissue sampling procedures, only cases delivered by cesarean section (CS) were included. Healthy women with normal pregnancies, undergoing CS for various reasons considered irrelevant to the aim of this study (e. g. breech presentation and previous CS), served as controls. Tissue was immediately submerged in a RNA stabilisation solution (RNAlater, Ambion, Huntingdon, U.K.), incubated at 4¡ãC overnight and stored at -80¡ãC
2007-08-31 | E-MEXP-1050 | biostudies-arrayexpress
Project description:Fibrosis are known as one of the characteristic pathological findings of placenta in preeclampsia (PE). The mechanism underlying tissue injury when placental stroma is exposed to hypoxia and inflammatory stimulation is unclear. We focused on the relationship between pathogenesis of PE and placental fibrosis, and investigated the changes of fibrosis related factors (FRFs) in placental stroma. The mRNA levels of fibrosis related factors in PE were higher than those in normal pregnancy (NP). Those under hypoxia and by TGF-β stimulation were more prominent in PE compared with NP. The contraction rate of PE had significantly higher than that of NP. The significant elevation of plasma level of TGF-β in PE was indicated compared with those in NP.
2017-05-18 | GSE99007 | 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:The risk of multiple placental thrombosis is increased in preeclampsia (PE) and vascular endothelium plays vital roles in coagulation such as secreting ITGA2B, vWF and TF. However, the pathological mechanism is unclear. Placental blood vessels were collected from PE and normal pregnancies. The protein level of ITGA2B was up-regulated in PE compared to the control, indicating enhanced coagulation function in the placenta of PE. Higher cholesterol levels and lower ALKBH1 expression were found in placental blood vessels of PE while the whole DNA N6-methyldeoxyadenosine levels (6mA) were up-regulated. However, DNA 6mA level of ITGA2B promoter was decreased. The Cholesterol overload experiment in human umbilical vein endothelial cells (HUVECs) showed that cholesterol regulated the protein expressions of ALKBH1 and ITGA2B, which was related to cholesterol concentration. ITGA2B protein expression was increased after ALKBH1 knockout. These data provide important information on cholesterol levels, ALKBH1 and ITGA2B expressions in coagulation function in placental blood vessels, which may be helpful for further investigations of potential targets and early prevention of placental thrombosis in PE.
2025-03-06 | GSE290312 | GEO