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. 2017 May 19;7:2210. doi: 10.1038/s41598-017-02056-w

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© The Author(s) 2017

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.

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IL22 contributed to the expression of STAT3 in the lung tissues in mice. Immunohistochemistry (A, B) indicated IL22 induced up-regulation of STAT3 in the lung tissues, but such fact was inhibited after AG490. The raw data were listed in the Supplementary file. (C) Western blot analysis indicated the expression of STAT3 in the lung tissues in the AngII+IL22 group was higher than the other groups. ^*P < 0.05 versus control group; ^#P < 0.05 versus AngII group and AngII+IL-22+AG490 group. The images of immunohistochemistry were observed under a magnification of 400× and 1000×, respectively.