Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
7
pubmed:dateCreated
2001-7-3
pubmed:abstractText
The integrity of cerebral microvessels requires the close apposition of the endothelium to the astrocyte endfeet. Integrins alpha1beta1 and alpha6beta4 are cellular matrix receptors that may contribute to cerebral microvascular integrity. It has been hypothesized that focal ischemia alters integrin expression in a characteristic time-dependent manner consistent with neuron injury. The effects of middle cerebral artery occlusion (MCAO) and various periods of reperfusion on microvasclar integrin alpha1beta1 and alpha6beta4 expression were examined in the basal ganglia of 17 primates. Integrin subunits alpha1 and beta1 colocalized with the endothelial cell antigen CD31 in nonischemic microvessels and with glial fibrillary acidic protein on astrocyte fibers. Rapid, simultaneous, and significant disappearance of both integrin alpha1 and beta1 subunits and integrin alpha6beta4 occurred by 2 hours MCAO, which was greatest in the region of neuron injury (ischemic core, Ic), and progressively less in the peripheral (Ip) and nonischemic regions (N). Transcription of subunit beta1 mRNA on microvessels increased significantly in the Ic/Ip border and in multiple circular subregions within Ic. Microvascular integrin alpha1beta1 and integrin alpha6beta4 expression are rapidly and coordinately lost in Ic after MCAO. With loss of integrin alpha1beta1, multiple regions of microvascular beta1 mRNA up-regulation within Ic suggest that microvessel responses to focal ischemia are dynamic, and that multiple cores, not a single core, are generated. These changes imply that microvascular integrity is modified in a heterogeneous, but ordered pattern.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
835-46
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed-meshheading:11435796-Animals, pubmed-meshheading:11435796-Antigens, CD31, pubmed-meshheading:11435796-Antigens, Surface, pubmed-meshheading:11435796-Astrocytes, pubmed-meshheading:11435796-Gene Expression, pubmed-meshheading:11435796-Glial Fibrillary Acidic Protein, pubmed-meshheading:11435796-Immunohistochemistry, pubmed-meshheading:11435796-In Situ Hybridization, pubmed-meshheading:11435796-Integrin alpha1beta1, pubmed-meshheading:11435796-Integrin alpha6beta4, pubmed-meshheading:11435796-Integrins, pubmed-meshheading:11435796-Ischemic Attack, Transient, pubmed-meshheading:11435796-Male, pubmed-meshheading:11435796-Microcirculation, pubmed-meshheading:11435796-Microscopy, Confocal, pubmed-meshheading:11435796-Middle Cerebral Artery, pubmed-meshheading:11435796-Neurons, pubmed-meshheading:11435796-Papio, pubmed-meshheading:11435796-RNA, Messenger
pubmed:year
2001
pubmed:articleTitle
Rapid loss of microvascular integrin expression during focal brain ischemia reflects neuron injury.
pubmed:affiliation
Department of Molecular and Experimental Medicine, The Scripps Research Institute, La Jolla, California, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't