The dose-dependent H2O2 stress response promotes increased survival for Schizosaccharomyces pombe cells expressing HIV-1 Vpr
Language English Country United States Media print
Document type Journal Article
PubMed
17176760
DOI
10.1007/bf02931584
Knihovny.cz E-resources
- MeSH
- Cell Cycle physiology MeSH
- vpr Gene Products, Human Immunodeficiency Virus MeSH
- Gene Products, vpr drug effects genetics metabolism MeSH
- HIV-1 genetics MeSH
- Humans MeSH
- Oxidative Stress physiology MeSH
- Hydrogen Peroxide pharmacology MeSH
- Cell Proliferation MeSH
- Schizosaccharomyces metabolism virology MeSH
- Cell Survival MeSH
- Dose-Response Relationship, Drug MeSH
- Check Tag
- Humans MeSH
- Publication type
- Journal Article MeSH
- Names of Substances
- vpr Gene Products, Human Immunodeficiency Virus MeSH
- Gene Products, vpr MeSH
- Hydrogen Peroxide MeSH
Human immunodeficiency virus type 1 (HIV-1) viral protein R (Vpr) exerts multiple effects on viral and host cellular activities during infection, including induction of the cell cycle G2 arrest, and cell death in both human cells and the fission yeast Schizosaccharomyces pombe. We show that treament of exponential-phase wild-type Vpr-expressing S. pombe cells with a low, subinhibitory concentration (0.15 mmol/L) of hydrogen peroxide and 0.1 mmol/L thiamine significantly increased both cell proliferation and survival rates and decreased the number of elongated G2-arrested cells. Short-term, H2O2-induced adaptive stress increased the survival of the cells while acute stress conditions interrupted the Vpr-mediated death of the cells; however, no changes in cell length or cell phase were detected. The results suggest the importance of the oxidative status of the cells in Vpr-mediated processes. Our findings contribute to the development of a new approach via which to investigate the contribution of Vpr to HIV pathogenesis and to reduce the Vpr-mediated effects in HIV-infected patients.
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Eur J Biochem. 1993 Jul 15;215(2):213-9 PubMed
Nucleic Acids Res. 2001 Jul 15;29(14 ):3030-40 PubMed
J Virol. 2000 Mar;74(6):2636-46 PubMed
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Mol Biol Cell. 1998 Jun;9(6):1339-49 PubMed
Antioxid Redox Signal. 2000 Fall;2(3):551-73 PubMed
Mol Biol Cell. 2001 Feb;12 (2):407-19 PubMed
AIDS. 2005 Oct 14;19(15):1555-64 PubMed
J Virol. 1999 Apr;73(4):3236-45 PubMed
J Virol. 2003 Apr;77(7):3962-72 PubMed
Environ Toxicol Pharmacol. 2003 Dec;15(1):19-26 PubMed
Cell Biol Int. 2005 Jan;29(1):57-63 PubMed
Nature. 1993 Mar 25;362(6418):355-8 PubMed
J Immunol. 2001 Sep 1;167(5):2743-52 PubMed
Folia Microbiol (Praha). 1993;38(6):524-6 PubMed
J Virol. 2001 Apr;75(8):3791-801 PubMed
J Gen Microbiol. 1993 Jul;139(7):1627-34 PubMed
J Virol. 1999 Feb;73(2):1447-52 PubMed
J Biol Chem. 1995 Nov 24;270(47):28457-62 PubMed
Genes Dev. 1998 May 15;12 (10 ):1391-7 PubMed
Mol Biol Cell. 2002 Mar;13(3):805-16 PubMed
Genes Dev. 1999 Jul 1;13(13):1653-63 PubMed
J Exp Med. 2001 Feb 19;193(4):F11-4 PubMed
Histol Histopathol. 2005 Jul;20(3):957-67 PubMed
J Virol. 2004 Sep;78(18):9697-704 PubMed
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Genes Cells. 1998 Aug;3(8):485-98 PubMed
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Methods Enzymol. 1991;194:795-823 PubMed
Ann Intern Med. 1996 Apr 1;124(7):654-63 PubMed
J Exp Med. 2005 Nov 21;202(10):1349-61 PubMed
Folia Microbiol (Praha). 2004;49(6):718-24 PubMed
Adv Microb Physiol. 2004;49:1-76 PubMed
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Front Biosci. 2002 Feb 01;7:d349-57 PubMed
J Virol. 2004 Oct;78(20):11016-29 PubMed
