Dataset Information

Proteomic profiling of extracellular vesicles from Nodal KO and control mouse placentas

ABSTRACT: This study evaluates the potential of placental extracellular vesicles (EVs) as biomarkers of midgestational pregnancy complications using a mouse model. EVs were isolated from embryonic day 10.5 (E10.5) placentas of control and uterine-specific Nodal knockout mice. Proteomic analyses revealed dysregulated molecules related to placental development, angiogenesis, and immune modulation. Several identified EV cargo components have known associations with complications such as IUGR and preeclampsia. These results suggest that placental EVs can reflect impaired placentation and may support early, non-invasive diagnostic strategies for reproductive disorders.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Placenta, Trophoblast Cell

DISEASE(S): Pre-eclampsia

SUBMITTER: parinaz kazemi

LAB HEAD: Daniel Dufort

PROVIDER: PXD065500 | Pride | 2025-08-25

REPOSITORIES: Pride

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	Ctl_31f5f15d6936b9399___Ctl_3.mgf.export.F012954.mzid_Ctl_3_1f5f15d6936b9399___Ctl_3.mgf.export.F012954.MGF	Mzid
	Ctrl_1aef9b87cedf1f80d___Ctrl_1.mgf.export.F012031.mzid	Mzid
	Ctrl_1aef9b87cedf1f80d___Ctrl_1.mgf.export.F012031.mzid_Ctrl_1_aef9b87cedf1f80d___Ctrl_1.mgf.export.F012031.MGF	Mzid
	Ctrl_2aef9b87cedf1f80d___Ctrl_2.mgf.export.F012032.mzid	Mzid

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Publications

Extracellular vesicles as prospective biological indicators for midgestational placental complications in the mouse.

Lee Elaine E Kazemi Parinaz P Shafiei Shiva S Yull Sarah S Rana Mansuba M Tawil Nadim N Montermini Laura L Rak Janusz J Dufort Daniel D

Frontiers in cell and developmental biology 20250724

<h4>Background</h4>Placental dysfunction is often associated with reproductive complications such as preeclampsia, intrauterine growth restriction (IUGR), and preterm birth. Currently, the early diagnosis and intervention of these pathologies remain challenging due to the invasive nature of placental tissue sampling. Liquid biopsies of extracellular vesicles (EVs) released from the placenta have emerged as a prospective minimally invasive diagnostic strategy that could provide insight into the m ...[more]

PMID: 40778264

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Project description:Background: Acute coronary syndromes (ACS) are associated with aberrant gene expression and epigenetic mechanisms. In particular, de novo DNA methylation is typically linked to gene silencing, but its role in heart disease remains not fully understood. Extracellular vesicles (EVs) are active components in cellular communication for their ability to carry a plethora of signalling biomolecules, thus representing a promising new diagnostic/therapeutic approach in cardiovascular diseases (CVDs). Indeed, there is the need of novel biomarkers for ACS prediction and timely detection. Purpose: We hypothesized that specific epigenetic signals can be carried by EVs. In this regard, we isolated and characterized circulating EVs from ACS patients and evaluated their potential role to influence DNA methylation in target cells. Methods: Circulating EVs were recovered, by ultracentrifugation, from plasma samples of 19 ACS patients and 50 healthy subjects (HS). Nanoparticle tracking analysis (NTA) and western blot (WB) were used to confirm the EVs integrity and purity. Peripheral blood mononuclear cells (PBMCs) of volunteer donors were treated with both ACS and HS derived EVs and genomic DNA was extracted to perform epigenome wide analysis through Reduced Representation Bisulfite Sequencing. ShinyGO, PANTHER, and STRING tools were interrogated to perform GO and PPI network analyses. Flow Cytometry, qRT-PCR, and WB analysis were also performed to evaluate and validate both intra-vesicular and intra-cellular signals. Results: Plasma ACS-derived EVs showed a significant up-regulation of DNA methyltransferases (DNMTs) gene expression levels as compared to HS (P<0.001). Specifically, de novo methylation transcripts, as DNMT3A and DNMT3B were significantly increased in plasma ACS-EVs. DNA methylation analysis of PBMCs from volunteer donors treated with HS- and ACS-derived EVs showed that RNF166 and CCND3 genes resulted the most hyper- and hypo-methylated, respectively, after by ACS-EV treatment. In addition, PPI network analysis specifically evidenced the subnetwork with SRC, as a hub gene, connecting it to NOTCH1, FOXO3, CDC42, IKBKG, RXRA, DGKG, known as important genes already involved in the onset of CVDs. Surprising, other novel genes, BAIAP2, SYP, CHL1, and SHB, which were hypomethylated, were found significantly overexpressed in PBMCs (P<0.005), underlying the fundamental modulating properties of EV cargo in atherosclerosis. Conclusions: These findings support the significant role of ACS plasma-derived EVs, inducing de novo DNA methylation signals, and modulating specific signaling pathways in target cells.