Journal
MICROVASCULAR RESEARCH
Volume 60, Issue 1, Pages 55-69Publisher
ACADEMIC PRESS INC
DOI: 10.1006/mvre.2000.2244
Keywords
pericyte; urokinase plasminogen activator; endothelial cell; traumatic brain injury; microvessels; apoptosis; migration
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Funding
- NINDS NIH HHS [5 P01 NS31287-05] Funding Source: Medline
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Any perturbation of the blood brain barrier, whether from changes in cell physiology or from direct injury, may result in microvascular dysfunction and disease. We examined, at the ultrastructural level, microvascular pericyte responses in a well-defined model of traumatic brain injury in the rat. In areas close to the site of impact cortical pericytes underwent a number of changes within the first hour. Approximately 40% of pericytes migrated from their microvascular location. Migration occurred concomitant with a thinning of the abluminal surface of the basal lamina and an accumulation of the receptor for the urokinase plasminogen activator on the leading surface of the migrating cell. Migrated pericytes appeared viable and remained in a perivascular location in the adjacent neuropil. Nonmigrating pericytes in the same section displayed cytoplasmic alterations and nuclear chromatin changes consistent with a rapid degenerative process. (C) 2000 Academic Press.
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