Linked Life Data

9782337

Source:http://linkedlifedata.com/resource/pubmed/id/9782337

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:dateCreated
1999-1-13
pubmed:abstractText
In the present study we have investigated the possibility that strain specific differences in the induction of apoptosis in macrophages could play a role in the resistance of strain A/J mice to MHV-3 induced hepatitis. MHV-3 infected macrophages from Balb/c and A/J mice were analyzed at various time points after infection. Apoptosis in A/J macrophages could be detected at 8 h post infection and increased significantly by 12 h, when almost 50-70% of the infected cells were undergoing apoptosis. In Balb/c macrophages, apoptotic changes were less pronounced and were observed in only 5-10% of the cells. MHV-3 induced apoptosis was inversely correlated with the ability of this virus to induce expression of fgl-2 prothrombinase protein and syncytia formation. Infected macrophages from A/J mice did not express fgl-2 protein and did not form syncytia. In contrast, infection of Balb/c derived macrophages resulted in fgl-2 expression and extensive syncytia formation. These data fit a model in which apoptosis of virally infected cells is a protective response which eliminates cells whose survival might be harmful for the whole organism.
pubmed:grant
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:issn
0065-2598
pubmed:author
pubmed:issnType
Print
pubmed:volume
440
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
619-25
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed:year
1998
pubmed:articleTitle
The pattern of induction of apoptosis during infection with MHV-3 correlates with strain variation in resistance and susceptibility to lethal hepatitis.
pubmed:affiliation
Department of Pathology and Laboratory Medicine, Texas A&M University College of Medicine, College Station 77843-1114, USA.
pubmed:publicationType
Journal Article, Research Support, U.S. Gov't, P.H.S., Research Support, Non-U.S. Gov't