title: Why and how to target angiogenesis in focal epilepsies.
abstract: We previously reported that blood-brain barrier (BBB) disruption was associated with a pathologic angiogenesis in patients with intractable temporal lobe epilepsy (TLE) and in vivo models. This was confirmed by the overexpression of vascular endothelial growth factor (VEGF) in neurons and astrocytes and of its receptor vascular endothelial growth factor-2 (VEGF-R2) (or flk1) in endothelial cells. Using an original in vitro model, we showed that seizures were sufficient to activate the VEGF/VEGF-R2 system, which promotes vascularization and tight junction disassembly. Such a BBB dysfunction was shown to contribute to epileptogenesis. Therefore, we postulate that drugs that target the specific VEGF-R2 pathways involved in permeability are able to repair the BBB, and, therefore, could reduce epileptogenicity.
authors.affiliation: Institute of Genomics Functional, CNRS UMR 5203, INSERM U661, University Montpellier 1&2, Montpellier, France. mireille.lerner-natoli@igf.cnrs.fr
authors.forename: Mélanie
authors.initials: M
authors.lastname: Morin-Brureau
authors.forename: Valérie
authors.initials: V
authors.lastname: Rigau
authors.forename: Mireille
authors.initials: M
authors.lastname: Lerner-Natoli
mesh_terms: D020533:Angiogenesis Inhibitors / Q000627:therapeutic use*; D000818:Animals; D001812:Blood-Brain Barrier / Q000187:drug effects* / Q000503:physiopathology*; D004828:Epilepsies, Partial / Q000188:drug therapy* / Q000503:physiopathology*; D004833:Epilepsy, Temporal Lobe / Q000188:drug therapy / Q000503:physiopathology; D006801:Humans; D009389:Neovascularization, Pathologic / Q000188:drug therapy / Q000503:physiopathology
chemical_list: D020533:Angiogenesis Inhibitors