Document Detail

Induction of programmed cell death by parvovirus H-1 in U937 cells: connection with the tumor necrosis factor alpha signalling pathway.
MedLine Citation:
PMID:  9765434     Owner:  NLM     Status:  MEDLINE    
The human promonocytic cell line U937 undergoes apoptosis upon treatment with tumor necrosis factor alpha (TNF-alpha). This cell line has previously been shown to be very sensitive to the lytic effect of the autonomous parvovirus H-1. Parvovirus infection leads to the activation of the CPP32 ICE-like cysteine protease which cleaves the enzyme poly(ADP-ribose)polymerase and induces morphologic changes that are characteristic of apoptosis in a way that is similar to TNF-alpha treatment. This effect is also observed when the U937 cells are infected with a recombinant H-1 virus which expresses the nonstructural (NS) proteins but in which the capsid genes are replaced by a reporter gene, indicating that the induction of apoptosis can be assigned to the cytotoxic nonstructural proteins in this cell system. The c-Myc protein, which is overexpressed in U937 cells, is rapidly downregulated during infection, in keeping with a possible role of this product in mediating the apoptotic cell death induced by H-1 virus infection. Interestingly, four clones (designated RU) derived from the U937 cell line and selected for their resistance to H-1 virus (J. A. Lopez-Guerrero et al., Blood 89:1642-1653, 1997) failed to decrease c-Myc expression upon treatment with differentiation agents and also resisted the induction of cell death after TNF-alpha treatment. Our data suggest that the RU clones have developed defense strategies against apoptosis, either by their failure to downregulate c-Myc and/or by activating antiapoptotic factors.
B Rayet; J A Lopez-Guerrero; J Rommelaere; C Dinsart
Related Documents :
21381154 - Granulocyte-macrophage colony stimulating factor blockade promotes ccr9(+) lymphocyte e...
21344504 - Ah receptor antagonism inhibits constitutive and cytokine inducible il6 production in h...
21398644 - Wnt pathway activation, cell migration, and lipid uptake is regulated by low-density li...
19158834 - The stem cell factor-c-kit pathway must be inhibited to enable apoptosis induced by bcr...
23750784 - A call to order at the spirochaetal host-pathogen interface.
3055214 - Complement and infectious agents.
Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Journal of virology     Volume:  72     ISSN:  0022-538X     ISO Abbreviation:  J. Virol.     Publication Date:  1998 Nov 
Date Detail:
Created Date:  1998-11-05     Completed Date:  1998-11-05     Revised Date:  2013-04-18    
Medline Journal Info:
Nlm Unique ID:  0113724     Medline TA:  J Virol     Country:  UNITED STATES    
Other Details:
Languages:  eng     Pagination:  8893-903     Citation Subset:  IM    
Angewandte Tumorvirologie, Abteilung F0100, Deutsches Krebsforschungszentrum, and Virologie Appliquée à l'Oncologie (Unité INSERM 375), D-69009 Heidelberg, Germany.
Export Citation:
APA/MLA Format     Download EndNote     Download BibTex
MeSH Terms
Apoptosis / drug effects,  physiology*
Caspases / metabolism
Enzyme Activation
Genes, myc
Parvovirus / genetics,  pathogenicity*
Poly(ADP-ribose) Polymerases / metabolism
Recombination, Genetic
Signal Transduction
Tumor Necrosis Factor-alpha / pharmacology,  physiology*
U937 Cells
Reg. No./Substance:
0/Tumor Necrosis Factor-alpha; EC Polymerases; EC 3.4.22.-/Caspases

From MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine

Previous Document:  A functional role for neutralizing antibodies in Borna disease: influence on virus tropism outside t...
Next Document:  Factors influencing adeno-associated virus-mediated gene transfer to human cystic fibrosis airway ep...