Journal article
Interleukin-11 links oxidative stress and compensatory proliferation
T Nishina, S Komazawa-Sakon, S Yanaka, X Piao, DM Zheng, JH Piao, Y Kojima, S Yamashina, E Sano, T Putoczki, T Doi, T Ueno, J Ezaki, H Ushio, M Ernst, K Tsumoto, K Okumura, H Nakano
Science Signaling | AMER ASSOC ADVANCEMENT SCIENCE | Published : 2012
Abstract
Apoptotic cells can stimulate the compensatory proliferation of surrounding cells to maintain tissue homeostasis. Although oxidative stress is associated with apoptosis and necrosis, whether it contributes to compensatory proliferation is unknown. Here, we showed that interleukin-11 (IL-11), a member of the IL-6 family of proinflammatory cytokines, was produced by cells in an oxidative stress-dependent manner. IL-11 production depended on the activation in dying cells of extracellular signal-regulated kinase 2, which in turn caused the phosphorylation and accumulation of the transcription factor Fra-1 by preventing its proteasome-dependent degradation. Fra-1 was subsequently recruited to the..
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Awarded by Japan Society for the Promotion of Science
Funding Acknowledgements
This work was supported in part by Grants-in-Aid for "High-Tech Research Center" Project for Private Universities: matching fund subsidy from the Ministry of Education, Culture, Sports, Science and Technology (MEXT); the Science Research Promotion Fund from the Promotion and Mutual Aid Corporation for Private Schools of Japan; Scientific Research (B) from Japan Society for the Promotion of Science; Scientific Research on innovative areas, MEXT, Japan; the Takeda Science Foundation; Astellas Foundation for Research on Metabolic Disorders; the National Health and Medical Research Council of Australia; and the Operational Infrastructure Support Program provided by the Victorian government. Author contributions: T.N., S.K.-S., S. Yanaka, X.P., D.-M.Z., J.-H.P., Y.K., S. Yamashina, E.S., and T.P. performed experiments; T.N., T.U., J.E., H.U., M.E., K.T., K.O., and H.N. designed the experiments and analyzed the data; T.D. and M.E. provided critical reagents; and H.N. wrote the paper.