Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
4
pubmed:dateCreated
2004-4-19
pubmed:abstractText
Oligodendrocytes, the myelin-forming cells of the CNS, are specifically sensitive to oxidative stress and respond by the onset of programmed cell death (PCD). To further unravel the molecular events underlying their enhanced susceptibility, we have investigated whether mitochondrial damage occurs during oxidative stress-induced PCD in cultured rat brain oligodendrocytes. Mitochondria are considered as a central control point of apoptosis, and mitochondrial dysfunction has been linked to neurodegenerative disease. Upon a number of stimuli through the release of cytochrome c, they coordinate caspase activation, causing morphological and biochemical changes associated with PCD. Oxidative stress was exerted by the application of hydrogen peroxide. The data show that hydrogen peroxide-induced apoptosis in oligodendrocytes involves mitochondrial damage and cytochrome c release and is accompanied by the activation of the death-related caspases 3 and 9. Concomitantly, the activation and nuclear translocation of extracellular signal regulated kinases ERK1,2 are observed, which have been implicated to participate in the regulation of cell death and survival. DNA fragmentation could not be attenuated by the ERK1,2 inhibitor PD 98059, indicating that the ERK1,2- pathway in oligodendrocytes may be involved in the initial survival response after exposure to stressful stimuli.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
May
pubmed:issn
0894-1491
pubmed:author
pubmed:copyrightInfo
Copyright 2004 Wiley-Liss, Inc.
pubmed:issnType
Print
pubmed:volume
46
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
446-55
pubmed:dateRevised
2009-11-19
pubmed:meshHeading
pubmed-meshheading:15095374-Animals, pubmed-meshheading:15095374-Animals, Newborn, pubmed-meshheading:15095374-Apoptosis, pubmed-meshheading:15095374-Caspases, pubmed-meshheading:15095374-Causality, pubmed-meshheading:15095374-Cells, Cultured, pubmed-meshheading:15095374-Cytochromes c, pubmed-meshheading:15095374-Demyelinating Diseases, pubmed-meshheading:15095374-Enzyme Inhibitors, pubmed-meshheading:15095374-Hydrogen Peroxide, pubmed-meshheading:15095374-Mitochondria, pubmed-meshheading:15095374-Mitogen-Activated Protein Kinases, pubmed-meshheading:15095374-Oligodendroglia, pubmed-meshheading:15095374-Oxidants, pubmed-meshheading:15095374-Oxidative Phosphorylation, pubmed-meshheading:15095374-Oxidative Stress, pubmed-meshheading:15095374-Rats, pubmed-meshheading:15095374-Rats, Wistar, pubmed-meshheading:15095374-Signal Transduction
pubmed:year
2004
pubmed:articleTitle
Mitochondrial pathway is involved in hydrogen-peroxide-induced apoptotic cell death of oligodendrocytes.
pubmed:affiliation
Department of Biology, Molecular Neurobiology, University of Oldenburg, Oldenburg, Germany.
pubmed:publicationType
Journal Article