Linked Life Data

11333363

Source:http://linkedlifedata.com/resource/pubmed/id/11333363

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
2001-5-2
pubmed:abstractText
In a rat forebrain ischemia model, the authors examined whether loss of cytochrome c from mitochondria correlates with ischemic hippocampal CA1 neuronal death and how cytochrome c release may shape neuronal death. Forebrain ischemia was induced by bilateral common carotid artery occlusion with simultaneous hypotension for 10 minutes. After reperfusion, an early rapid depletion of mitochondrial cytochrome c and a late phase of diffuse redistribution of cytochrome c occurred in the hippocampal CA1 region, but not in the dentate gyrus and CA3 regions. Intracerebroventricular administration of Z-DEVD-FMK, a relatively selective caspase-3 inhibitor, provided limited but significant protection against ischemic neuronal damage on day 7 after reperfusion. Treatment with 3 minutes of ischemia (ischemic preconditioning) 48 hours before the 10-minute ischemia attenuated both the early and late phases of cytochrome c redistribution. In another subset of animals treated with cycloheximide, a general protein synthesis inhibitor, the late phase of cytochrome c redistribution was inhibited, whereas most hippocampal CA1 neurons never regained mitochondrial cytochrome c. Examination of neuronal survival revealed that ischemic preconditioning prevents, whereas cycloheximide only delays, ischemic hippocampal CA1 neuronal death. DNA fragmentation detected by terminal deoxytransferase-mediated dUTP-nick end labeling (TUNEL) in situ was largely attenuated by ischemic preconditioning and moderately reduced by cycloheximide. These results indicate that the loss of cytochrome c from mitochondria correlates with hippocampal CA1 neuronal death after transient cerebral ischemia in relation to both caspase-dependent and -independent pathways. The amount of mitochondrial cytochrome c regained may determine whether ischemic hippocampal CA1 neurons survive or succumb to late-phase death.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0271-678X
pubmed:author
pubmed:issnType
Print
pubmed:volume
21
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
529-40
pubmed:dateRevised
2006-11-15
pubmed:meshHeading
pubmed-meshheading:11333363-Animals, pubmed-meshheading:11333363-Apoptosis, pubmed-meshheading:11333363-Blotting, Western, pubmed-meshheading:11333363-Caspase 3, pubmed-meshheading:11333363-Caspases, pubmed-meshheading:11333363-Cycloheximide, pubmed-meshheading:11333363-Cytochrome c Group, pubmed-meshheading:11333363-DNA Fragmentation, pubmed-meshheading:11333363-Enzyme Inhibitors, pubmed-meshheading:11333363-Fluorescent Antibody Technique, pubmed-meshheading:11333363-Hippocampus, pubmed-meshheading:11333363-In Situ Nick-End Labeling, pubmed-meshheading:11333363-Ischemic Preconditioning, pubmed-meshheading:11333363-Male, pubmed-meshheading:11333363-Mitochondria, pubmed-meshheading:11333363-Neurons, pubmed-meshheading:11333363-Oligopeptides, pubmed-meshheading:11333363-Prosencephalon, pubmed-meshheading:11333363-Protein Synthesis Inhibitors, pubmed-meshheading:11333363-Rats, pubmed-meshheading:11333363-Rats, Wistar, pubmed-meshheading:11333363-Vasospasm, Intracranial
pubmed:year
2001
pubmed:articleTitle
Both caspase-dependent and caspase-independent pathways may be involved in hippocampal CA1 neuronal death because of loss of cytochrome c From mitochondria in a rat forebrain ischemia model.
pubmed:affiliation
Department of Anesthesiology, Niigata University School of Medicine, Niigata, Japan.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't