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Why and how to target angiogenesis in focal epilepsies
Author(s) -
MorinBrureau Mélanie,
Rigau Valérie,
LernerNatoli Mireille
Publication year - 2012
Publication title -
epilepsia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.687
H-Index - 191
eISSN - 1528-1167
pISSN - 0013-9580
DOI - 10.1111/j.1528-1167.2012.03705.x
Subject(s) - neuroscience , epilepsy , medicine , psychology
Summary 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.