VEGFR-2 expression in brain injury: its distribution related to brain-blood barrier markers

VEGF is a major regulator of angiogenesis and vascular permeability in development and injury. The involvement of one of its receptors, Flk-1 in angiogenesis has been widely demonstrated, but few studies elucidate its role as a mediator of the BBB permeability and none displays its distribution foll...

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Bibliographic Details
Published in:Journal of Neural Transmission 2006-04, Vol.113 (4), p.487-496
Main Authors: Lafuente, J V, Argandoña, E G, Mitre, B
Format: Article
Language:English
Subjects:
Animals
Astrocytes - metabolism
Biomarkers - analysis
Blood-Brain Barrier - metabolism
Blood-Brain Barrier - pathology
Brain Injuries - metabolism
Brain Injuries - pathology
Capillary Permeability - physiology
Endothelial Cells - metabolism
Immunohistochemistry
Necrosis - metabolism
Necrosis - pathology
Neurons - metabolism
Rats
Rats, Sprague-Dawley
Vascular Endothelial Growth Factor Receptor-2 - biosynthesis
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Summary:VEGF is a major regulator of angiogenesis and vascular permeability in development and injury. The involvement of one of its receptors, Flk-1 in angiogenesis has been widely demonstrated, but few studies elucidate its role as a mediator of the BBB permeability and none displays its distribution following a cortical micronecrosis. A microvascular marker (LEA lectin), two BBB markers (EBA, GluT-1) and the VEGFR2 receptor were studied in adult rats after a minimal brain injury. Immunohistochemistry shows an increase of positive vessels, somata and processes around the micronecrosis from 6 to 72 hours after injury. Flk-1 was overexpressed mainly in endothelial cells, but also in astrocytes, neuronal somata and processes adjacent to the damage. This increase correlates to the lose of positivity for EBA. After injury, VEGFR-2 expression increases and its distribution corresponds to VEGF one. The whole system seems to play a role in the disruption of the BBB.
ISSN:0300-9564
1435-1463
DOI:10.1007/s00702-005-0407-0