Activité, Système Moteur & Coordination
Douleur - Allodynie/Hyperalgésie Thermique
Douleur - Spontanée - Déficit de Posture
Douleur - Allodynie/Hyperalgésie Mécanique
Anxiété & Dépression
Apprentissage/Mémoire - Attention - Addiction
Physiologie & Recherche Respiratoire
Métabolisme & Prise Alimentaire
Douleur
Système Nerveux Central (SNC) 
Neurodégénérescence
Système sensoriel
Système moteur
Troubles de l'humeur
Autres pathologies
Système musculaire
Articulations
Métabolisme
Thématiques transversales
Bioseb on booth #14 at OARSI 2024 in Vienna Authors
Treps L, Edmond S, Harford-Wright E, Galan-Moya EM, Schmitt A, Azzi S, Citerne A, Bidère N, Ricard D, Gavard J
Lab
CNRS, UMR8104, Paris, France.
Journal
Oncogene.
Abstract
Glioblastoma are malignant highly vascularized brain tumours, which feature large oedema resulting from tumour-promoted vascular leakage. The pro-permeability factor Semaphorin3A (Sema3A) produced within glioblastoma has been linked to the loss of endothelial barrier integrity. Here, we report that extracellular vesicles (EVs) released by patient-derived glioblastoma cells disrupt the endothelial barrier. EVs expressed Sema3A at their surface, which accounted for in vitro elevation of brain endothelial permeability and in vivo vascular permeability, in both skin and brain vasculature. Blocking Sema3A or its receptor Neuropilin1 (NRP1) hampered EV-mediated permeability. In vivo models using ectopically and orthotopically xenografted mice revealed that Sema3A-containing EVs were efficiently detected in the blood stream. In keeping with this idea, sera from glioblastoma multiforme (GBM) patients also contain high levels of Sema3A carried in the EV fraction that enhanced vascular permeability, in a Sema3A/NRP1-dependent manner. Our results suggest that EV-delivered Sema3A orchestrates loss of barrier integrity in glioblastoma and may be of interest for prognostic purposes.Oncogene advance online publication, 14 September 2015; doi:10.1038/onc.2015.317.