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. 2014 May 22;5(5):e1238. doi: 10.1038/cddis.2014.207

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Copyright © 2014 Macmillan Publishers Limited

Cell Death and Disease is an open-access journal published by Nature Publishing Group. This work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 Unported License. The images or other third party material in this article are included in the article's Creative Commons license, unless indicated otherwise in the credit line; if the material is not included under the Creative Commons license, users will need to obtain permission from the license holder to reproduce the material. To view a copy of this license, visit http://creativecommons.org/licenses/by-nc-nd/3.0/

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Enhancement of miR-26a expression attenuates EMT in vitro and in vivo. (a) miR-26a suppresses the TGF-β1-induced increase in collagen content in A549 cells. Western blot (b) and immunofluorescence (c) assays found that miR-26a suppresses TGF-β1-induced EMT in A549 cells. (d) Administration of agomiR-26a attenuates collagen content in bleomycin-treated mice, whereas agomiR-NC has no effect. Western blot (e) and immunofluorescence (f) assays shows that agomiR-26a attenuates EMT in the lungs of mice with pulmonary fibrosis. E-cadherin is stained in green, Vimentin is in red and the nuclei are in blue (magnification, 200 × ). n=4; *P<0.05 versus control, #P<0.05 versus TGF-β1; **P<0.01 versus saline, ^##P<0.01 versus BLM