Note to users. If you're seeing this message, it means that your browser cannot find this page's style/presentation instructions -- or possibly that you are using a browser that does not support current Web standards. Find out more about why this message is appearing, and what you can do to make your experience of our site the best it can be.


Sci. Signal., 17 January 2012
Vol. 5, Issue 207, p. ra5
[DOI: 10.1126/scisignal.2002056]


Editor's Summary

Dying Cells Protect the Neighborhood
In addition to releasing a number of factors that induce the production of proinflammatory cytokines, dying cells can promote wound healing and tissue homeostasis by inducing the proliferation of surrounding cells in a process known as compensatory proliferation. Nishina et al. found that in dying hepatocytes reactive oxygen species triggered the production of the cytokine interleukin-11 (IL-11), which induced the proliferation of surrounding cells by activating the transcription factor STAT3. Consistent with these in vitro findings, IL-11 signaling protected hepatocytes in a mouse model of acetaminophen-induced liver injury, and mice deficient in a component of the IL-11 receptor had exacerbated disease. Together, these findings suggest that IL-11 stimulates compensatory proliferation in response to oxidative stress.

Citation: T. Nishina, S. Komazawa-Sakon, S. Yanaka, X. Piao, D.-M. Zheng, J.-H. 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, Interleukin-11 Links Oxidative Stress and Compensatory Proliferation. Sci. Signal. 5, ra5 (2012).

Read the Full Text

c-FLIP Maintains Tissue Homeostasis by Preventing Apoptosis and Programmed Necrosis.
X. Piao, S. Komazawa-Sakon, T. Nishina, M. Koike, J.-H. Piao, H. Ehlken, H. Kurihara, M. Hara, N. Van Rooijen, G. Schutz, et al. (2012)
Science Signaling 5, ra93
   Abstract »    Full Text »    PDF »

To Advertise     Find Products

Science Signaling. ISSN 1937-9145 (online), 1945-0877 (print). Pre-2008: Science's STKE. ISSN 1525-8882