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B-to plasma-cell terminal differentiation entails oxidative stress and profound reshaping of the antioxidant responses

Title
B-to plasma-cell terminal differentiation entails oxidative stress and profound reshaping of the antioxidant responses
Authors
Bertolotti M.Yim S.H.Garcia-Manteiga J.M.Masciarelli S.Kim Y.-J.Kang M.-H.Iuchi Y.Fujii J.Vene R.Rubartelli A.Rhee S.G.Sitia R.
Ewha Authors
이서구임선희
SCOPUS Author ID
이서구scopusscopus
Issue Date
2010
Journal Title
Antioxidants and Redox Signaling
ISSN
1523-0864JCR Link
Citation
vol. 13, no. 8, pp. 1133 - 1144
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Limited amounts of reactive oxygen species are necessary for cell survival and signaling, but their excess causes oxidative stress. H2O 2 and other reactive oxygen species are formed as byproducts of several metabolic pathways, possibly including oxidative protein folding in the endoplasmic reticulum. B-to plasma-cell differentiation is characterized by a massive expansion of the endoplasmic reticulum, finalized to sustain abundant immunoglobulin (Ig) synthesis and secretion. The increased production of disulfide-rich Ig might cause oxidative stress that could serve signaling roles in the differentiation and lifespan control of antibody-secreting cells. Here we show that terminal B-cell differentiation entails redox stress, NF-E2-related factor-2 (Nrf2) activation, and reshaping of the antioxidant responses. However, plasma-cell differentiation was not dramatically impaired in peroxiredoxin (Prx)1-, 2-, 3-, and 4-, glutathione peroxidase 1-, and Nrf2-knockout splenocytes, suggesting redundancy and robustness in antioxidant systems. Endoplasmic reticulum (ER)-resident Prx4 increases dramatically during differentiation. In its absence, IgM secretion was not significantly affected, but more high-molecular-weight covalent complexes accumulated intracellularly. Our results suggest that the early intracellular production of H 2O2 facilitates B-cell proliferation and reveal a role for the Nrf2 pathway in the differentiation and function of IgM-secreting cells. © 2010, Mary Ann Liebert, Inc.
DOI
10.1089/ars.2009.3079
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일반대학원 > 생명·약학부 > Journal papers
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