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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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Inhibition of DEX-Ac induced OHT in mice after Ad5.hGRβ overexpression. Weekly periocular CF injections of DEX-Ac in both eyes significantly elevated IOP in mice. Nighttime IOP measurements were performed between different treatment groups of mice- DEX-Ac (n = 18), Vehicle (n = 10), DEX-Ac + Ad5.hGRβ (n = 18) and DEX-Ac + Ad5.null (n = 12). GRβ transduction of the TM at day 18 after DEX-Ac induced IOP elevation significantly lowered IOP within 7 days to baseline IOPs and remained at baseline throughout the end of the study, thus reversing GC-OHT in mouse eyes. Data are presented as means ± SEM. ^####P < 0.0001 (DEX-Ac versus Ad5.hGRβ), ⁺⁺⁺⁺P < 0.0001 (DEX-Ac + Ad5.hGRβ versus DEX-Ac + Ad5.null), and ****P < 0.0001 (DEX-Ac versus vehicle and vehicle versus DEX-Ac, DEX-Ac + Ad5.hGRβ, DEX-Ac + Ad5.null until day 18), One-way ANOVA.