Format

Send to

Choose Destination
J Neural Transm (Vienna). 2006 Apr;113(4):487-96.

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

Author information

1
Laboratory of Clinical and Experimental Neuroscience (LaNCE), Department of Neuroscience, University of the Basque Country, Leioa, Spain. onplasav@lg.ehu.es

Abstract

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.

PMID:
16550327
DOI:
10.1007/s00702-005-0407-0
[Indexed for MEDLINE]

Supplemental Content

Full text links

Icon for Springer
Loading ...
Support Center