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Involvement of the vascular wall in regenerative processes after CA1 ischemic neuronal death
Author(s) -
SalazarColocho Pablo,
Del Río Joaquín,
Frechilla Diana
Publication year - 2008
Publication title -
international journal of developmental neuroscience
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.761
H-Index - 88
eISSN - 1873-474X
pISSN - 0736-5748
DOI - 10.1016/j.ijdevneu.2008.05.008
Subject(s) - neurogenesis , dentate gyrus , gerbil , ischemia , biology , vascular endothelial growth factor , hippocampus , neuroscience , colocalization , neun , bromodeoxyuridine , fibroblast growth factor , pathology , microbiology and biotechnology , anatomy , medicine , immunology , cancer research , immunohistochemistry , vegf receptors , biochemistry , receptor
The involvement of vascular wall in response to neuronal death was challenged here using a transient forebrain ischemia model in gerbil, which causes CA1 neuronal death and trigger neurogenesis in hippocampus. We found an important vascular reaction in CA1 5 days after ischemia evaluated by Von Willebrand factor and Vimentin immunoreactivity, as well as increased expression of angiogenic and neurogenic regulators: Vascular endothelial growth factor (VEGF) and fibroblast growth factor‐2 (FGF‐2). Analysing the morphology and cell phenotype by confocal microscopy, we confirmed the colocalization of the neurogenic markers (bromodeoxyuridine–neuronal nuclei–TOPRO‐3) in newborn cells associated to vascular walls in CA1 and dentate gyrus of hippocampus 32 days after ischemia. The results indicate that vascular tissues may participate in neurogenesis after brain ischemia, reinforce the notion that blood vessels represent a source of neuronal progenitor cells in damaged brain areas and suggest that molecular and cellular manipulation of the vascular wall may expand the possibilities of novel regenerative therapies.