Hierarchical control of interleukin 13 (IL-13) signals in lung fibroblasts by STAT6 and SOX11

Yasutaka Mitamura, Satoshi Nunomura, Yasuhiro Nanri, Kazuhiko Arima, Tomohito Yoshihara, Kosaku Komiya, Shogo Fukuda, Hiroaki Takatori, Hiroshi Nakajima, Masutaka Furue, Kenji Izuhara

Research output: Contribution to journalArticlepeer-review

25 Citations (Scopus)


Interleukin (IL)-13 is a signature cytokine of type 2 inflammation important for the pathogenesis of various diseases, including allergic diseases. Signal transducer and activator of transcription (STAT) 6 is a critical transcriptional factor for the IL-13 signals; however, it remains unknown how expression of the IL-13–induced genes is differentiated by the transcriptional machineries. In this study, we identified IL-13–induced transcriptional factors in lung fibroblasts using DNA microarrays in which SOX11 was included. Knockdown of SOX11 down-regulated expression of periostin and CCL26, both of which are known to be downstream molecules of IL-13, whereas enforced expression of SOX11 together with IL-13 stimulation enhanced expression of periostin. Moreover, we found that in DNA microarrays combining IL-13 induction and SOX11 knockdown there exist both SOX11-dependent and -independent molecules in IL-13–inducible molecules. In the former, many inflammation-related and fibrosis-related molecules, including periostin and CCL26, are involved. These results suggest that SOX11 acts as a trans-acting transcriptional factor downstream of STAT6 and that in lung fibroblasts the IL-13 signals are hierarchically controlled by STAT6 and SOX11.

Original languageEnglish
Pages (from-to)14646-14658
Number of pages13
JournalJournal of Biological Chemistry
Issue number38
Publication statusPublished - Sept 21 2018

All Science Journal Classification (ASJC) codes

  • Biochemistry
  • Molecular Biology
  • Cell Biology


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