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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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Comparison of conventional outflow facility (C) between DEX-Ac, vehicle, and DEX-Ac + Ad5.hGRβ-treated mice. After 6 weeks of treatment, DEX-Ac (n = 14) significantly decreased the C compared to vehicle (n = 13) treated mice. GRβ transduction (DEX-Ac + Ad5.hGRβ; n = 13) returned the outflow facility to normal levels compared to DEX-Ac treated mice. Data are presented as means ± SEM. *P < 0.05, **P < 0.01. One-Way ANOVA.