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. 2018 Jan 16;8:862. doi: 10.1038/s41598-018-19262-9

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© The Author(s) 2018

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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DEX-Ac + Ad5.hGRβ treatment decreased expression of fibronectin (FN), collagen I (Col I), and myocilin (MYOC) in the anterior segment of the mouse eyes. Representative western blot image of fibronectin (FN), collagen I (Col I), and myocilin (MYOC) in the anterior segment tissue lysates of DEX-Ac, vehicle, and DEX-Ac + Ad5.hGRβ treated mice. DEX-Ac treatment increased FN, Col I, and MYOC expression, which returned to normal control levels in DEX-Ac + Ad5.hGRβ treated mice. GAPDH served as loading control. Representative data from following anterior segments per group: DEX-Ac n = 3; DEX-Ac + Ad5.hGRβ n = 3; vehicle n = 2. Please refer Supplementary Figures 4, 5, 6, and 7 for full-length blots as representative image is cropped.