Linked Life Data

3793799

Source:http://linkedlifedata.com/resource/pubmed/id/3793799

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
6
pubmed:dateCreated
1987-1-27
pubmed:abstractText
This study examined the pattern of protein synthesis in the neocortex, caudate-putamen, and the hippocampus following transient forebrain ischemia in rats. The animal model of temporary ischemia used in this study causes permanent damage to vulnerable neurons with a time course of injury that varies from hours (caudate nucleus) to days (hippocampus). To examine the spectrum of proteins synthesized in these regions at 3 and 18 h after recirculation, cerebral proteins were pulse-labeled in vivo by an intravenous injection of [35S]methionine. Newly synthesized (35S-labeled) and constitutive (unlabeled) proteins were analyzed by two-dimensional gel electrophoresis and fluorography. In all three brain regions, specific proteins underwent preferential synthesis (Mr approximately 27,000, approximately 65,000, approximately 70,000, approximately 110,000), while others showed decreased synthesis (neuron-specific enolase, alpha- and beta-tubulin). There was an early (3 h post ischemia) induction of the Mr approximately 70,000 mammalian "stress" protein; at 18 h post ischemia, its synthesis remained high in the hippocampus but was diminished in the neocortex and had largely subsided in the caudate-putamen. All regions at 18 h showed increased synthesis of an Mr approximately 50,000 protein, tentatively identified as glial fibrillary acidic protein. The results show that temporary forebrain ischemia induces changes in protein synthesis that include features similar to those observed in other eukaryotic cells subjected to injurious stress. These postischemic changes in protein synthesis are qualitatively similar in all brain regions examined despite regional differences in the severity of subsequent neuronal damage. The persistent synthesis of the Mr approximately 70,000 stress protein in the hippocampus, however, may reflect continued metabolic injury long after the ischemic episode has passed.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Dec
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
6
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
642-9
pubmed:dateRevised
2007-11-14
pubmed:meshHeading
pubmed:year
1986
pubmed:articleTitle
Protein synthesis in postischemic rat brain: a two-dimensional electrophoretic analysis.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't