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Herjan, Tomasz; Yao, Peng; Qian, Wen; Li, Xiao; Liu, Caini; Bulek, Katarzyna; Sun, Dongxu; Yang, Wen-Pin; Zhu, Jun; He, Aiqing; Carman, Julie A; Erzurum, Serpil C; Lipshitz, Howard D; Fox, Paul L; Hamilton, Thomas A; Li, Xiaoxia
The Journal of immunology (1950), 07/2013, Volume: 191, Issue: 2Journal Article
IL-17, a major inflammatory cytokine plays a critical role in the pathogenesis of many autoimmune inflammatory diseases. In this study, we report a new function of RNA-binding protein HuR in IL-17-induced Act1-mediated chemokine mRNA stabilization. HuR deficiency markedly reduced IL-17-induced chemokine expression due to increased mRNA decay. Act1-mediated HuR polyubiquitination was required for the binding of HuR to CXCL1 mRNA, leading to mRNA stabilization. Although IL-17 induced the coshift of Act1 and HuR to the polysomal fractions in a sucrose gradient, HuR deficiency reduced the ratio of translation-active/translation-inactive IL-17-induced chemokine mRNAs. Furthermore, HuR deletion in distal lung epithelium attenuated IL-17-induced neutrophilia. In summary, HuR functions to couple receptor-proximal signaling to posttranscriptional machinery, contributing to IL-17-induced inflammation.
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