Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Proteomic analysis of bronchial smooth muscle cells extracellular vesicles

ABSTRACT: The main objective of CHARMACOMA is to explore the capacity of the severe asthmatic bronchial smooth muscle to modify bronchial epithelium physiology from a metabolic point of view.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human)

TISSUE(S): Bronchus Smooth Muscle

SUBMITTER: Dupuy Jean-William

LAB HEAD: Pauline Esteves

PROVIDER: PXD055968 | Pride | 2025-11-26

REPOSITORIES: Pride

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
	Link_between_files.xlsx	Xlsx
	RP_UP000005640_Homo_sapiens_2023_09_13.fasta	Fasta
	checksum.txt	Txt
	pe210308_01.msf	Msf
	pe210308_01.pdResult	Other

Items per page:

1 - 5 of 57

Publications

Bronchial smooth muscle extracellular vesicles interfere with bronchial epithelium metabolism and function in asthma.

Celle Elisa E Chahin Amine A Beaufils Fabien F Cardouat Guillaume G Eyraud Edmée E Bouchet Clément C Campagnac Marilyne M Ousova Olga O Begueret Hugues H Thumerel Matthieu M Dubois Rémi R Dupuy Jean-William JW Leste-Lasserre Thierry T Lacomme Sabrina S Lager-Lachaud Nina N Bellvert Floriant F Marthan Roger R Girodet Pierre-Olivier PO Berger Patrick P Trian Thomas T Esteves Pauline P

iScience 20250429 6

Bronchial smooth muscle (BSM) remodeling is an important feature of severe asthma pathophysiology. We previously showed that asthmatic BSM is metabolically different and increased rhinovirus (RV) replication rate, the main trigger of severe asthma exacerbations. Extracellular vesicles (EVs) are the key mediator in cell-cell communication, but the role of BSM cells-derived EVs on bronchial epithelial has never been investigated in asthma. Using severe asthmatic and non-asthmatic tissue collection ...[more]

PMID: 40487443

Similar Datasets

Proteomic analysis of lungs in early experimental model of Chronic obstructive pulmonary disease (COPD)

Project description:Rationale: Chronic obstructive pulmonary disease (COPD) is a prevalent respiratory disease lacking disease modifying treatment. The role of CXCL12/CXCR4 axis has been demonstrated in acute exacerbation of COPD. The interest of study early COPD has been recently pointed out. Objectives: To study the role of the CXCL12/CXCR4 axis in both human and mouse model of early COPD. Methods: Blood and lung tissue were obtained from both COPD patients and mice exposed to cigarette smoke (CS) for 10 weeks and intranasal instillations of polyinosinic–polycytidylic acid (poly(I:C)) to mimic exacerbations for 5 weeks. Measurements and Main Results: Exposed mice presented mild airway obstruction, peri-bronchial fibrosis and right heart remodeling. The level of CXCR4 expressing cells was increased in the blood of exposed mice, as well as in the blood of patients with mild COPD. Lung CXCL12 expression was higher both in exposed mice and COPD patients. The densities of fibrocytes expressing CXCR4 were increased in the blood and in the bronchial submucosa of exposed mice. Conditional inactivation of CXCR4 at adult stage as well as pharmacological inhibition of CXCR4 with plerixafor injections improved lung function and inflammation and protected against CS and poly-(I:C)-induced airway and cardiac remodeling. CXCR4-/- and plerixafor-treated mice also had reduced levels of CXCR4-expressing circulating cells and a lower density of peri-bronchial fibrocytes. Conclusions: We demonstrated that targeting CXCR4 has beneficial effects in an animal model of early COPD, and provide a framework to translate preclinical findings to clinical settings within a drug repurposing approach.

2025-05-12 | PXD040105 | Pride

Short-range interactions between fibrocytes and CD8+ T cells in COPD bronchial inflammatory response

Project description:The peri-bronchial zone of chronic obstructive pulmonary disease (COPD) is the site of extensive infiltration of immune cell, allowing persistent contacts between resident cells and immune cells. Tissue fibrocytes interaction with CD8+ T cells and its consequences were investigated. We show that fibrocytes and CD8+ T cells are found in vicinity in distal airways and that potential interactions are more frequent in tissues from COPD patients compared to those of control subjects. Increased proximity and clusterization between CD8+ T cells and fibrocytes are associated with altered lung function. Tissular CD8+ T cells from COPD patients promote fibrocyte chemotaxis via the CXCL8-CXCR1/2 axis. CD8+ T cells establish short-term interactions with fibrocytes, that trigger CD8+ T cell proliferation in a CD54- and CD86-dependent manner, pro-inflammatory cytokines production, CD8+ T cell cytotoxic activity and fibrocyte immunologic signaling. We defined a computational model describing these intercellular interactions and calibrated the parameters based on our experimental measurements. We showed the model’s ability to reproduce histological ex vivo characteristics, and observed major contributions of fibrocyte-mediated CD8+ T cell proliferation and fibrocyte death in COPD development. Using the model to test therapeutic scenarios, we predicted a recovery time of several years, and the failure of targeting independently chemotaxis or interacting processes. Altogether, our study reveals that local interactions between fibrocytes and CD8+ T cells can occur in vivo and could jeopardize the balance between protective immunity and chronic inflammation in bronchi of COPD patients.

2023-07-28 | PXD041402 | Pride

Combining laser capture micro-dissection and proteomics reveals an active translation machinery controlling invadosome formation

Project description:We developed a method that combines laser micro-dissection and mass spectrometry, enabling the analysis of subcellular structures in their native state based on low amounts of input material. Using this combinatorial method, we showed that invadosomes contain specific components of the translational machinery, in addition to known marker proteins.

2018-10-19 | PXD009390 | Pride

Proteomic analysis of BioID experiments performed with Toxoplasma gondii MyoJ protein tagged with TurboID in tachyzoites

Project description:The aim of the project was to identify proteins of the basal complex of Toxoplasma gondii using MyoJ as bait

2022-11-01 | PXD035106 | Pride

Proteomic analysis of Src cells treated with the Src inhibitor PP2

Project description:This project is focus on the role of Src signaling involved in translation related to invadosome formation. The aim of this project is to decipher the molecular mechanism involved in specific and local translation into invadosome.

2025-11-28 | PXD071367 | Pride

Analyses of FBXL6 interaction with newly synthesized proteins.

Project description:HEK cells were grown in light media for two weeks. One day before experiments, cells were transfected with FBXL6-flag or B-gal (control). At t=0, cells were switched to heavy media for 3h and then Flag immunoprecipitation were performed. Pulled down protein were analyzed by mass spectrometry.

2023-09-25 | PXD037602 | Pride

Proteomic analysis of WT and RagA-deficient macrophages that have phagocytosed SILAC-bacteria

Project description:Macrophage are phagocytic cells that reprogram their cellular metabolism depending on the nature of innate immune receptors engaged upon microbial encounter. Yet, whether engulfed microbes constitute a source of nutrients for macrophages and how this contribute at establishing a specific metabolic reprogramming is poorly defined. Our study aims at understanding how microbial-derived amino acids feed macrophage metabolism by tracing labelled microbial amino acid in macrophage proteins. Here we compared the incorporation of labelled amino acids derived from dead bacteria into macrophage proteins.

2025-04-18 | PXD058174 | Pride

Proteomic analysis of ConcanamycinA-treated macrophages that have phagocytosed SILAC-bacteria

2025-04-18 | PXD058147 | Pride

Proteomic analysis of macrophages that have phagocytosed SILAC -bacteria using a trans-well system

2025-04-18 | PXD058145 | Pride

Proteomic analysis of HepG2 cells after mutated ß-catenin depletion

Project description:ß-catenin is a main oncogene in a large number of cancers (colorectal, liver, melanoma, uterus). Local immunosuppression induced by certain cancers remains a major problem of resistance to immunotherapies and its molecular mechanism remains poorly understood. Recently, ß-catenin mutated tumors (hepatocellular carcinoma (HCC) and melanoma) have been described as promoting immune evasion and resistance to anti-PD1 immunotherapy. Based on preliminary data obtained in HCC, we hypothesize that a defect in intercellular communication could be the cause of this immune evasion. The main objective of this project is to identify proteomic signatures of factors that can induce this immune escape in ß-catenin mutated HCC such as exosomes.

2024-07-08 | PXD043841 | Pride