Linked Life Data

11476594

Source:http://linkedlifedata.com/resource/pubmed/id/11476594

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-7-30
pubmed:abstractText
Previous studies have shown that intracerebral administration of glial cell line-derived neurotrophic factor (GDNF) reduces ischemia-mediated cerebral infarction. The biological effects of GDNF are mediated by GDNF-family receptor alpha-1 (GFRalpha-1) and c-Ret. In this study, we examined the levels of expression of GFRalpha-1 and c-Ret in a rat model of stroke. Adult Sprague-Dawley rats were anesthetized with chloral hydrate. The right middle cerebral artery was ligated at its distal branch for 90 min. Animals were sacrificed at 0, 6, 12, and 24 h after reperfusion and levels of expression of GFRalpha-1 and c-Ret mRNA were determined by in situ hybridization histochemistry. We found that GFRalpha-1 mRNA was up-regulated in CA3, dentate gyrus (DG), cortex, and striatum. The peak of up-regulation in DG was 6 h after reperfusion. GFRalpha-1 mRNA levels in CA3 were gradually up-regulated over the 24-h reperfusion period. In cortex, GFRalpha-1 mRNA was up-regulated at all time points; however, the peak of up-regulation was observed at 0 and 24 h after reperfusion. In striatum, an initial up-regulation of GFRalpha-1 was found at 0 h after ischemia. In striatum, up-regulation of c-Ret mRNA was detected as early as 0 h after reperfusion. A gradual increase was found at 6, 12, and 24 h after reperfusion. In conclusion, our results indicate that there are both regional and temporal differences in up-regulation of GFRalpha-1 and c-Ret after ischemia. Since GDNF is neuroprotective, up-regulation of GFRalpha-1 and c-Ret could enhance the responsiveness to GDNF and reduce neuronal damage. The selective up-regulation of GFRalpha-1 and c-Ret in different brain areas suggests that there may be regional differences in GDNF-induced neuroprotection in stroke.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Aug
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
Copyright 2001 Academic Press.
pubmed:issnType
Print
pubmed:volume
170
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
283-9
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11476594-Analysis of Variance, pubmed-meshheading:11476594-Animals, pubmed-meshheading:11476594-Brain, pubmed-meshheading:11476594-Cerebral Cortex, pubmed-meshheading:11476594-Corpus Striatum, pubmed-meshheading:11476594-Dentate Gyrus, pubmed-meshheading:11476594-Disease Models, Animal, pubmed-meshheading:11476594-Drosophila Proteins, pubmed-meshheading:11476594-Gene Expression Regulation, pubmed-meshheading:11476594-Glial Cell Line-Derived Neurotrophic Factor Receptors, pubmed-meshheading:11476594-In Situ Hybridization, pubmed-meshheading:11476594-Ischemic Attack, Transient, pubmed-meshheading:11476594-Kinetics, pubmed-meshheading:11476594-Male, pubmed-meshheading:11476594-Middle Cerebral Artery, pubmed-meshheading:11476594-Organ Specificity, pubmed-meshheading:11476594-Proto-Oncogene Proteins, pubmed-meshheading:11476594-Proto-Oncogene Proteins c-ret, pubmed-meshheading:11476594-RNA, Messenger, pubmed-meshheading:11476594-Rats, pubmed-meshheading:11476594-Rats, Sprague-Dawley, pubmed-meshheading:11476594-Receptor Protein-Tyrosine Kinases, pubmed-meshheading:11476594-Reperfusion, pubmed-meshheading:11476594-Stroke, pubmed-meshheading:11476594-Time Factors, pubmed-meshheading:11476594-Transcription, Genetic
pubmed:year
2001
pubmed:articleTitle
Time course study of GFRalpha-1 expression in an animal model of stroke.
pubmed:affiliation
National Institute on Drug Abuse, National Institutes of Health, 5500 Nathan Shock Drive, Baltimore, Maryland 21224, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S.