期刊
JOURNAL OF CELL BIOLOGY
卷 175, 期 5, 页码 779-789出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1083/jcb.200606005
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- NHLBI NIH HHS [P01 HL067004, P01 HL67004] Funding Source: Medline
- NIEHS NIH HHS [T32 ES007122] Funding Source: Medline
- NIGMS NIH HHS [R01 GM74204, R01 GM074204, R01 GM050389, R01 GM050389-13] Funding Source: Medline
Inactivation of eukaryotic 2-Cys peroxiredoxins (Prxs) by hyperoxidation has been proposed to promote accumulation of hydrogen peroxide (H2O2) for redox-dependent signaling events. We examined the oxidation and oligomeric states of PrxI and -II in epithelial cells during mitogenic signaling and in response to fluxes of H2O2. During normal mitogenic signaling, hyperoxidation of PrxI and -II was not detected. In contrast, H2O2-dependent cell cycle arrest was correlated with hyperoxidation of PrxII, which resulted in quantitative recruitment of similar to 66- and similar to 140-kD PrxII complexes into large filamentous oligomers. Expression of cyclin D1 and cell proliferation did not resume until PrxII-SO2H was reduced and native PrxII complexes were regenerated. Ectopic expression of PrxI or -II increased Prx-SO2H levels in response to oxidant exposure and failed to protect cells from arrest. We propose a model in which Prxs function as peroxide dosimeters in subcellular processes that involve redox cycling, with hyperoxidation controlling structural transitions that alert cells of perturbations in peroxide homeostasis.
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