Linked Life Data

1908877

Source:http://linkedlifedata.com/resource/pubmed/id/1908877

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
5
pubmed:dateCreated
1991-9-27
pubmed:abstractText
The cytotoxic effect of recombinant human cytokines was tested on glial cells cultured from mature bovine brain. Lymphotoxin (LT) and TNF induced injury to oligodendrocytes in a time and dose-dependent fashion. The other cytokines tested, IFN-gamma, IL-6, and IL-2, did not affect oligodendrocytes in culture over a 72-h observation period. None of the cytokines injured astrocytes cultured from the same source. LT showed a much more potent cytotoxicity than TNF toward oligodendrocytes; cytotoxic changes were noted earlier (24 h) and at lower units of activity. Morphologic studies showed that the LT-mediated effects were associated with early retraction of cell processes, depolymerization of F-actin and subsequent nuclear degeneration. Lack of early cytoplasmic membrane injury as measured by 51Cr release and electron microscope studies demonstrating nuclear disintegration suggested an apoptotic mechanism of oligodendrocyte injury evoked by LT, which was supported by DNA integrity assay. These results demonstrate that LT possesses potent cytotoxic activity against oligodendrocytes and that the major mechanism involved in this process is DNA fragmentation.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Sep
pubmed:issn
0022-1767
pubmed:author
pubmed:issnType
Print
pubmed:day
1
pubmed:volume
147
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1522-9
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1991
pubmed:articleTitle
Cytokine cytotoxicity against oligodendrocytes. Apoptosis induced by lymphotoxin.
pubmed:affiliation
Department of Pathology (Neuropathology), Albert Einstein College of Medicine, Bronx, NY 10461.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't