Linked Life Data

11716555

Source:http://linkedlifedata.com/resource/pubmed/id/11716555

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2001-11-21
pubmed:abstractText
Signal transduction pathways that lead to the modulation of genes related to survival and repair mechanisms are activated in neurons that survive injury. These protein kinase/phosphatase cascades converge on transcription factors, the DNA binding proteins that directly regulate gene expression. In this study we examined expression of the NF-kappaB p50 subunit in the rat hippocampus 7 days after injury caused by middle cerebral artery occlusion or trimethyltin treatment. We found increased levels of p50 in neurons throughout the hippocampus after both treatments, localized not only in cell bodies but also in processes. At the 7-day time point, Fluoro-Jade histochemistry revealed hippocampal neurodegeneration in trimethyltin-treated rats but not in those lesioned by middle cerebral artery occlusion. p50 was not expressed in Fluoro-Jade-positive degenerating cells, supporting the role of this transcriptional subunit in neurosurvival. Because phosphorylation of the inhibitor IkappaB protein by IkappaB kinase is the classic step in NF-kappaB activation, phospho-IkappaBalpha immunoreactivity was examined as an indication of IkappaB kinase activity. Levels of phospho-IkappaBalpha were increased in neurons throughout the hippocampus 7 days postinjury. Immunoblotting for phospho-IkappaBalpha demonstrated increased levels 1 day postinjury that remained elevated for at least 7 days. These data suggest that NF-kappaB signal transduction is involved in an adaptive response of neurons that survive injury.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0014-4886
pubmed:author
pubmed:copyrightInfo
(c)2001 Elsevier Science.
pubmed:issnType
Print
pubmed:volume
172
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
307-19
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:11716555-Animals, pubmed-meshheading:11716555-Arterial Occlusive Diseases, pubmed-meshheading:11716555-Cell Survival, pubmed-meshheading:11716555-Cerebral Arteries, pubmed-meshheading:11716555-Fluorescent Dyes, pubmed-meshheading:11716555-Hippocampus, pubmed-meshheading:11716555-Histocytochemistry, pubmed-meshheading:11716555-I-kappa B Kinase, pubmed-meshheading:11716555-Immunoblotting, pubmed-meshheading:11716555-Male, pubmed-meshheading:11716555-NF-kappa B, pubmed-meshheading:11716555-NF-kappa B p50 Subunit, pubmed-meshheading:11716555-Nerve Degeneration, pubmed-meshheading:11716555-Neurons, pubmed-meshheading:11716555-Organic Chemicals, pubmed-meshheading:11716555-Protein-Serine-Threonine Kinases, pubmed-meshheading:11716555-Rats, pubmed-meshheading:11716555-Rats, Sprague-Dawley, pubmed-meshheading:11716555-Time Factors, pubmed-meshheading:11716555-Tissue Distribution, pubmed-meshheading:11716555-Trimethyltin Compounds
pubmed:year
2001
pubmed:articleTitle
NF-kappaB p50 is increased in neurons surviving hippocampal injury.
pubmed:affiliation
Department of Pharmacology and Therapeutics, University of South Florida, Tampa, Florida 33612, USA. kpennypa@hsc.usf.edu
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't