Document Detail


Parvovirus H-1-induced cell death: influence of intracellular NAD consumption on the regulation of necrosis and apoptosis.
MedLine Citation:
PMID:  10581389     Owner:  NLM     Status:  MEDLINE    
Abstract/OtherAbstract:
The autonomous parvovirus H-1 exerts tumor-suppressive effects in living organisms and has been shown to specifically interfere with the survival of transformed cells in culture. The mechanism(s) by which H-1 virus induces death of transformed cells is not yet well understood. It has recently been reported that H-1 virus induces apoptotic cell death in the human monocytic U937 cell line, as assessed by biochemical and morphological changes of infected cells (Rayet, B., Lopez-Guerrero, J.-A., Rommelaere, J., Dinsart, C., 1998. Induction of programmed cell death by parvovirus H-1 in U937 cells: connection with the TNFalpha signalling pathway. J. Virol. 72, 8893-8903). Here we show that parvovirus H-1 infection induced early biochemical changes pointing to apoptotic events also in the transformed human keratinocyte cell line, HeLa, and the transformed rat fibroblast cell line, P1. Morphologic changes, however, and in particular the early breakdown of plasma membrane integrity, suggested that apoptosis did not go to completion, leading to necrotic cell death as the major result of parvovirus infection of HeLa and P1 cells. Parvovirus infection of these, and to a significantly lesser extent of U937 cells, was accompanied by rapid depletion of intracellular NAD stores. Inhibition of NAD-consuming enzymes interfered with parvovirus-induced NAD depletion and increased the proportion of H-1 virus-infected cells displaying apoptotic features of cell death. In contrast, a similar prevention of NAD depletion through stimulation of NAD production had little influence on the cell death pathway, suggesting that NAD-consuming enzymes may promote necrosis in a direct way rather than through inducing the overall drop of intracellular NAD.
Authors:
Z Ran; B Rayet; J Rommelaere; S Faisst
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Publication Detail:
Type:  Journal Article; Research Support, Non-U.S. Gov't    
Journal Detail:
Title:  Virus research     Volume:  65     ISSN:  0168-1702     ISO Abbreviation:  Virus Res.     Publication Date:  1999 Dec 
Date Detail:
Created Date:  2000-02-01     Completed Date:  2000-02-01     Revised Date:  2006-11-15    
Medline Journal Info:
Nlm Unique ID:  8410979     Medline TA:  Virus Res     Country:  NETHERLANDS    
Other Details:
Languages:  eng     Pagination:  161-74     Citation Subset:  IM    
Affiliation:
Applied Tumor Virology Program, Abt. F0100 and Institut National de la Santé et de la Recherche Médicale U 375, Deutsches Krebsforschungszentrum, 69120, Heidelberg, Germany.
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MeSH Terms
Descriptor/Qualifier:
Animals
Apoptosis
Cell Death*
Cell Line
Cell Transformation, Viral
Fibroblasts
Hela Cells
Humans
Keratinocytes / enzymology,  pathology,  virology
NAD / metabolism*,  physiology*
Necrosis
Parvoviridae Infections / metabolism,  pathology
Parvovirus / genetics*
Rats
U937 Cells / enzymology,  pathology,  virology
Chemical
Reg. No./Substance:
53-84-9/NAD

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


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