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Iron mediates endothelial cell damage and blood-brain barrier opening in the hippocampus after transient forebrain ischemia in rats

Authors
Won, SM; Lee, JH; Park, UJ; Gwag, J; Gwag, BJ; Lee, YB
Citation
Experimental & molecular medicine, 43(2):121-128, 2011
Journal Title
Experimental & molecular medicine
ISSN
1226-36132092-6413
Abstract
Blood cells are transported into the brain and are thought to participate in neurodegenerative processes following hypoxic ischemic injury. We examined the possibility that transient forebrain ischemia (TFI) causes the blood-brain barrier (BBB) to become permeable to blood cells, possibly via dysfunction and degeneration of endothelial cells in rats. Extravasation of Evans blue and immunoglobulin G (IgG) was observed in the hippocampal CA1-2 areas within 8 h after TFI, and peaked at 48 h. This extravasation was accompanied by loss of tight junction proteins, occludin, and zonula occludens-1, and degeneration of endothelial cells in the CA1-2 areas. Iron overload and mitochondrial free radical production were evident in the microvessel endothelium of the hippocampus before endothelial cell damage occurred. Administration of deferoxamine (DFO), an iron chelator, or Neu2000, an antioxidant, blocked free radical production and endothelial cell degeneration. Our findings suggest that iron overload and iron-mediated free radical production cause loss of tight junction proteins and degeneration of endothelial cells, opening of the BBB after TFI.
MeSH terms
AnimalsBlood-Brain Barrier/*metabolismCapillary PermeabilityEndothelial Cells/*metabolismEvans Blue/metabolismFree Radicals/metabolismHippocampus/*metabolism/pathologyIron/*metabolismIschemic Attack, Transient/pathology/*physiopathologyMaleMembrane Proteins/metabolismRatsRats, Sprague-Dawley
DOI
10.3858/emm.2011.43.2.020
PMID
21278483
Appears in Collections:
Journal Papers > School of Medicine / Graduate School of Medicine > Pharmacology
Journal Papers > Research Organization > Institute for Medical Sciences
AJOU Authors
곽, 병주이, 용범
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