Dataset Information

Proteomics on mouse obese and non-obese visceral adipose tissue derived extracellular vesicles

ABSTRACT: Visceral adipose tissue (VAT) was harvested from wild-type mice fed high-fat diet to induce obesity or matched diet as non-obese controls. VAT was ex vivo cultured for 48 hrs and its conditioned media was collected. Extracellular vesicles were isolated from conditioned media by ultracentrifugation. The aim of the project was to characterize extracellular vesicle protein cargo from obese and non-obese VAT.

INSTRUMENT(S):

ORGANISM(S): Mus Musculus (mouse)

TISSUE(S): Cell Suspension Culture

SUBMITTER: Parsa Haque

LAB HEAD: Arianne Theiss

PROVIDER: PXD057432 | Pride | 2025-04-22

REPOSITORIES: Pride

ACCESS DATA

Dataset's files

Source:

			Action	DRS
	QEHF_20221226_PHaque_939MVMD.raw	Raw
	QEHF_20221226_PHaque_966FVHFD.raw	Raw
	QEHF_2022122_PHaque_1001MVHFD.raw	Raw
	QEHF_2022122_PHaque_820MVHFD.raw	Raw
	QEHF_2022122_PHaque_973975FVMD.raw	Raw

Items per page:

1 - 5 of 8

Publications

Obese Adipose Tissue Extracellular Vesicles Activate Mitochondrial Fatty Acid β-oxidation to Drive Colonic Stemness.

Haque Parsa S PS Goodman Desiree D Kuusivuori-Robinson Thor T Coughlan Christina C Delgado-Deida Yaritza Y Onyiah Joseph C JC Zempleni Janos J Theiss Arianne L AL

Cellular and molecular gastroenterology and hepatology 20250322 7

<h4>Background & aims</h4>Patients with obesity and mouse models of obesity exhibit abnormalities in intestinal epithelial cells, including enhanced stemness. Adipose tissue (AT) is the largest endocrine organ secreting cytokines, hormones, and extracellular vesicles (EVs). Here, we characterized EV protein cargo from obese and non-obese AT and demonstrate the role of obese adipose-derived EVs in enhancing colonic stemness.<h4>Methods</h4>EVs were isolated from visceral AT from mice fed high-fat ...[more]

PMID: 40122519

Similar Datasets

Project description:Rationale. Obesity is a risk factor for atherothrombosis and various cancers. However, the mechanisms are not completely uncovered. Objectives. We aimed to verify whether the microparticles (MPs) released from thrombin-activated platelets differed in obese and nonobese women for number, size, and proteomics cargo and the capacity to modulate in vitro the expression of genes related to the epithelial to mesenchymal transition (EMT) and the endothelial to mesenchymal transition (EndMT), and COX-2, a pro-angiogenic pathway. Methods and Results. MPs were obtained from thrombin activated platelets of four obese women and their matched, lean controls . MPs were analyzed by cytofluorimeter and protein content by liquid chromatography-mass spectrometry. Obese MPs were not different in number but were characterized by increased heterogeneity in size. In obese individuals, MPs containing mitochondria (mitoMPs) expressed lower CD41 levels and increased phosphatidylserine associated with enhanced Factor V representing a signature of a prothrombotic state. Proteomics analysis identified 44 proteins downregulated and 3 upregulated in obese versus nonobese MPs . A reduction in the proteins involved in mitophagy and antioxidant defenses, and of the -granular membrane was detected in the MPs of obese individuals. MPs released from platelets of obese individuals were more prone to induce the expression of marker genes of EMT and EndMT when incubated with HT29 cells and human cardiac microvascular endothelial cells(HCMEC), respectively. A protein, highly enhanced in obese MPs, was the pro-platelet basic protein with pro-inflammatory and tumorigenic actions. MPs from obese, but not nonobese, women induced COX-2 in HCMEC. Conclusions. Platelet-derived MPs of obese women showed higher heterogeneity in size and contained different levels of proteins relevant to thrombosis and tumorigenesis. Obese MPs presented enhanced capacity to induce changes in the expression of EMT and EndMT markers and COX-2. These effects might contribute to the increased risk for the development of thrombosis and multiple malignancies in obesity.