Regulation of peroxiredoxins by nitric oxide in immunostimulated macrophages
| Autor: | Blanche Guillon, Flora Tomasello, Simon Fourquet, Cécile Bouton, Kahina Abbas, Michel B. Toledano, Alexandre Diet, Jean-Claude Drapier |
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| Přispěvatelé: | Institut de Chimie des Substances Naturelles (ICSN), Centre National de la Recherche Scientifique (CNRS)-Institut de Chimie du CNRS (INC) |
| Rok vydání: | 2007 |
| Předmět: |
[SDV.BC]Life Sciences [q-bio]/Cellular Biology
Oxidative phosphorylation Biology Nitric Oxide Biochemistry Gene Expression Regulation Enzymologic Nitric oxide Cell Line 03 medical and health sciences chemistry.chemical_compound Mice 0302 clinical medicine Peroxynitrous Acid Animals Molecular Biology 030304 developmental biology chemistry.chemical_classification Mice Knockout 0303 health sciences Reactive oxygen species Messenger RNA Regeneration (biology) Macrophages Cell Biology Hydrogen Peroxide Peroxiredoxins Oxidants 3. Good health Cell biology Up-Regulation Sulfiredoxin Oxidative Stress chemistry Signal transduction Oxidation-Reduction 030217 neurology & neurosurgery Peroxynitrite Peroxiredoxin VI Signal Transduction |
| Zdroj: | Journal of Biological Chemistry Journal of Biological Chemistry, American Society for Biochemistry and Molecular Biology, 2007, 282 (50), pp.36199-205. ⟨10.1074/jbc.M706420200⟩ |
| ISSN: | 0021-9258 1083-351X |
| DOI: | 10.1074/jbc.M706420200⟩ |
| Popis: | International audience; Reactive oxygen species and nitric oxide (NO) are capable of both mediating redox-sensitive signal transduction and eliciting cell injury. The interplay between these messengers is quite complex, and intersection of their signaling pathways as well as regulation of their fluxes requires tight control. In this regard, peroxiredoxins (Prxs), a recently identified family of six thiol peroxidases, are central because they reduce H(2)O(2), organic peroxides, and peroxynitrite. Here we provide evidence that endogenously produced NO participates in protection of murine primary macrophages against oxidative and nitrosative stress by inducing Prx I and VI expression at mRNA and protein levels. We also show that NO prevented the sulfinylation-dependent inactivation of 2-Cys Prxs, a reversible overoxidation that controls H(2)O(2) signaling. In addition, studies using macrophages from sulfiredoxin (Srx)-deficient mice indicated that regeneration of 2-Cys Prxs to the active form was dependent on Srx. Last, we show that NO increased Srx expression and hastened Srx-dependent recovery of 2-Cys Prxs. We therefore propose that modulation by NO of Prx expression and redox state, as well as up-regulation of Srx expression, constitutes a novel pathway that contributes to antioxidant response and control of H(2)O(2)-mediated signal transduction in mammals. |
| Databáze: | OpenAIRE |
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