Hepatitis c virus infection induces pro- and antiapoptotic cell response: who is the winner?

Détails

ID Serval
serval:BIB_313B32B1CBFE
Type
Actes de conférence (partie): contribution originale à la littérature scientifique, publiée à l'occasion de conférences scientifiques, dans un ouvrage de compte-rendu (proceedings), ou dans l'édition spéciale d'un journal reconnu (conference proceedings).
Sous-type
Abstract (résumé de présentation): article court qui reprend les éléments essentiels présentés à l'occasion d'une conférence scientifique dans un poster ou lors d'une intervention orale.
Collection
Publications
Institution
Titre
Hepatitis c virus infection induces pro- and antiapoptotic cell response: who is the winner?
Titre de la conférence
35th Congress of the Federation of European Biochemical Societies
Auteur(s)
Ripoli M., Quarato G., Scrima R., D'Aprile A., Pazienza V., Boffoli D., Moradpour D., Capitanio N., Piccoli C.
Adresse
Gothenburg, Sweden, June 26-July 1, 2010
ISBN
1742-464X
Statut éditorial
Publié
Date de publication
2010
Peer-reviewed
Oui
Volume
277
Série
FEBS Journal
Pages
101
Langue
anglais
Notes
Meeting Abstract
Résumé
Introduction:
Apoptosis plays a central role in chronic hepatitis C virus (HCV) infection. Although the activation of cell death signals has been reported, HCV infection persists in most patients suggesting a pro-survival adaptation, eventually developing hepatocellular carcinoma. This study focused on the role of mitochondria in the activation of pro- and antiapoptotic response in cells expressing HCV proteins. Materials and Methods: Human Osteosarcoma U2-OS cells inducibly expressing the HCV polyprotein; huh7.5 hepatoma cells transfected with full length HCV genome.
Results:
Long term induction of viral proteins in U2-OS cells induced a cyclosporine A-sensitive cytochrome c partial release from mitochondria, revealed by immunofluorescence, western blot and spectral analysis. In HCV-transfected Huh7.5 cells, release of the apoptosis inducing factor (AIF) with no apparent nuclear translocation was also observed. HCV positive cells displayed
an HIF-dependent enhanced glycolysis, charachterized by up-regulation of the mitochondria-bound Hexokinase II (HKII); preliminary data on signal transduction pathway revealed the iperphosphorylation of Glycogen synthase kinase 3b(GSK3b).
Conclusion:
HCV causes a cell stress activating an early apoptotic response, the entity of which likely depends on the cell type. Nevertheless a wide series of cell survival mechanisms are also
triggered resulting in a metabolic adaptation possibly favouring carcinogenesis. Based on our results, we propose a pro-survival mechanism linking HCV infection to inhibition of GSK-3b, stabilization of HIF1a and up-regulation of HKII, the last events causing a glycolytic shift and protecting from apoptosis.
Web of science
Création de la notice
08/09/2010 15:30
Dernière modification de la notice
20/08/2019 13:16
Données d'usage