Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
1996-1-26
pubmed:abstractText
Cortical brain damage was produced in rats by a focal pulse from a Nd-YAG laser, and evolution of the lesion was evaluated at 30 min, and 2, 8, and 24 h with respect to microvascular perfusion, blood-brain barrier (BBB) permeability, and expression of both the heat-shock/stress protein, hsp72, and the c-fos proto-oncogene transcription factor. A double-labeling fluorescence technique employing intravenously injected Evans blue albumin (EBA) and fluorescein-labeled dextran was used to map and measure BBB damage and microvascular perfusion in fresh frozen brain sections. Hsp72 and c-fos mRNAs were localized by in situ hybridization, and the respective proteins were identified by immunocytochemistry. Parallel sections were stained for glial fibrillary acidic protein and for routine histologic examination. Striking hsp72 mRNA expression was evident by 2 h in an approximately 300 microns wide rim surrounding an area of expanding BBB damage. Increased hsp72 mRNA was observed only in regions of preserved microcirculation, where the hsp72 protein was subsequently localized exclusively in the vasculature at 24 h after the insult. Hsp72-positive endothelial cells spanned the narrow margin between the lesion and histologically normal, glial fibrillary acidic protein (GFAP)-positive cortical tissue. There was no hsp72 expression in the area of subcortically migrating edema fluid. Inductions of c-fos mRNA and Fos protein were not strikingly evident around the focal brain lesion, but were observed transiently throughout the injured hemisphere at 30 min and 2.5 h, respectively, indicating that spreading depression was triggered by the focal injury. These results are in striking contrast to those previously obtained from studies of models of focal ischemic or traumatic brain injury, which are characterized by a complex pattern of glial and neuronal hsp72 expression in the periphery of an infarct, and which suggest that the tightly demarcated lesion produced by the Nd-YAG laser lacks these components of graded injury that are evident following other types of focal brain damage.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jan
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
16
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
82-91
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:8530560-Animals, pubmed-meshheading:8530560-Base Sequence, pubmed-meshheading:8530560-Blood-Brain Barrier, pubmed-meshheading:8530560-Brain Chemistry, pubmed-meshheading:8530560-Brain Injuries, pubmed-meshheading:8530560-Cerebral Cortex, pubmed-meshheading:8530560-Cerebrovascular Circulation, pubmed-meshheading:8530560-Endothelium, Vascular, pubmed-meshheading:8530560-Glial Fibrillary Acidic Protein, pubmed-meshheading:8530560-HSP72 Heat-Shock Proteins, pubmed-meshheading:8530560-Heat-Shock Proteins, pubmed-meshheading:8530560-Immunohistochemistry, pubmed-meshheading:8530560-In Situ Hybridization, pubmed-meshheading:8530560-Male, pubmed-meshheading:8530560-Microcirculation, pubmed-meshheading:8530560-Microscopy, Fluorescence, pubmed-meshheading:8530560-Molecular Sequence Data, pubmed-meshheading:8530560-Proto-Oncogene Proteins c-fos, pubmed-meshheading:8530560-RNA, Messenger, pubmed-meshheading:8530560-Rats, pubmed-meshheading:8530560-Rats, Sprague-Dawley
pubmed:year
1996
pubmed:articleTitle
Heat-shock protein and C-fos expression in focal microvascular brain damage.
pubmed:affiliation
Department of Neurology, University of Helsinki, Finland.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't