Interleukin-11 Links Oxidative Stress and Compensatory Proliferation

Takashi Nishina, Sachiko Komazawa-Sakon, Saeko Yanaka, Xuehua Piao, Dong-Mei Zheng, Jiang-Hu Piao, Yuko Kojima, Shunhei Yamashina, Emiko Sano, Tracy Putoczki, Takahiro Doi, Takashi Ueno, Junji Ezaki, Hiroko Ushio, Matthias Ernst, Kouhei Tsumoto, Ko Okumura, Hiroyasu Nakano*

*To whom correspondence should be addressed. E-mail: hnakano{at}juntendo.ac.jp

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• Fig. S1. H₂O₂, but not TNF-α or LPS, induces IL-11 production in HepG2 cells.
• Fig. S2. t-BuOOH induces Il11 expression.
• Fig. S3. Il11 mRNA expression is increased in dying cells.
• Fig. S4. Activation of the ERK pathway is critical for Il11 mRNA expression in RelA^–/– MEFs and HepG2 cells.
• Fig. S5. The PI3K-Akt pathway partly contributes to the expression of Il11 mRNA.
• Fig. S6. Oxidative stress induces the formation of high–molecular mass oligomers of MKP3.
• Fig. S7. H₂O₂ activates the Il11 promoter in HCT116 cells.
• Fig. S8. Fra-1 interacts with ERK2.
• Fig. S9. The ROS-induced increased abundance of Fra-1 is not regulated at the level of mRNA.
• Fig. S10. Serum IL-11 concentrations are increased in mice after induction of severe hepatitis.
• Fig. S11. Amelioration of oxidative stress suppresses IL-11 production and phosphorylation of STAT3 in APAP-induced hepatitis.
• Fig. S12. Amelioration of oxidative stress suppresses IL-11 production and phosphorylation of STAT3 in hepatitis induced with antibody against Fas.
• Fig. S13. IL-11 is produced by hepatocytes upon oxidative stress.
• Fig. S14. The IL-11R agonist N_T-3N induces STAT3-dependent signals.
• Fig. S15. The IL-11R agonist N_T-3N ameliorates APAP-induced oxidative stress.
• Fig. S16. APAP-induced liver injury is not exacerbated in male Il11ra^–/– mice.
• Fig. S17. A model for apoptosis- and necrosis-induced compensatory proliferation.
• Table S1. Genes whose expression in H₂O₂-treated MEFs was increased compared to that in untreated MEFs.
  

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© 2012 American Association for the Advancement of Science