Linked Life Data

10215166

Source:http://linkedlifedata.com/resource/pubmed/id/10215166

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
1999-6-10
pubmed:abstractText
Expression of platelet-derived growth factor B-chain and of its specific receptor (beta-receptor) was investigated in immature brains with hypoxic/ischemic injury. After the left common carotid arteries of seven-day-old rats were ligated and pups were placed in a hypoxic chamber, the protein and messenger RNA of both B-chain and beta-receptor were assessed using immunocytochemistry and northern analysis, respectively. Transcripts for B-chain were localized by in situ hybridization. Faint but definite expression of B-chain and beta-receptor was seen in the brains of untreated neonatal controls. Three to 48 h after hypoxia B-chain protein was generally increased above control levels, but focally decreased expression was seen in infarcted areas. Enhanced induction of messenger RNA of B-chain was seen in the both sides of cerebral cortices and hippocampi at 3 h. Strongly increased positivity for B-chain protein and mRNA occurred in the neurons surrounding the infarct. In situ hybridization still showed this up-regulation seven days after hypoxia. Beta-receptor protein expression was enhanced in some neurons immediately surrounding the infarct at 3 h of hypoxia, and marked up-regulation was seen at 16 h. Beta-receptor messenger RNA remained at control levels. Immunocytochemistry showed strong immunoreactivity for the beta-receptor on the neurons surrounding the infarct at 72 h. These results indicate that a neonatal hypoxic/ischemic insult induces neuronal up-regulation of the platelet-derived growth factor B-chain as well as beta-receptor immediately after hypoxia. While this up-regulation is relatively transient in most neurons, sublethal damage to neurons immediately surrounding an infarct induces sustained up-regulation. Through autocrine and paracrine mechanisms, platelet-derived growth factor B-chain molecules may act as a neuroprotective factor in immature brain experiencing with hypoxic/ischemic injury.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0306-4522
pubmed:author
pubmed:issnType
Print
pubmed:volume
90
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
643-51
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:10215166-Animals, pubmed-meshheading:10215166-Animals, Newborn, pubmed-meshheading:10215166-Cerebral Infarction, pubmed-meshheading:10215166-Gene Expression Regulation, pubmed-meshheading:10215166-Hypoxia, Brain, pubmed-meshheading:10215166-Immunohistochemistry, pubmed-meshheading:10215166-In Situ Hybridization, pubmed-meshheading:10215166-Ischemic Attack, Transient, pubmed-meshheading:10215166-Macromolecular Substances, pubmed-meshheading:10215166-Neurons, pubmed-meshheading:10215166-Platelet-Derived Growth Factor, pubmed-meshheading:10215166-Rats, pubmed-meshheading:10215166-Rats, Sprague-Dawley, pubmed-meshheading:10215166-Receptor, Platelet-Derived Growth Factor beta, pubmed-meshheading:10215166-Receptors, Platelet-Derived Growth Factor, pubmed-meshheading:10215166-Time Factors, pubmed-meshheading:10215166-Transcription, Genetic
pubmed:year
1999
pubmed:articleTitle
Expression of platelet-derived growth factor B-chain and beta-receptor in hypoxic/ischemic encephalopathy of neonatal rats.
pubmed:affiliation
Department of Pediatrics, Shiga University of Medical Science, Otsu, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't