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. 2017 Sep 6;7:10716. doi: 10.1038/s41598-017-10719-x

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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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Cavtratin protects RGCs against injury in the acute ocular hypertension model. (A,B) Cavtratin decreased the number of apoptotic cells in the retina. AP or cavtratin was injected into the vitreous chamber 4 hr before the acute ocular hypertension treatment. Retinae were collected 3d after the hypertension. Fewer TUNEL⁺ cells were detected in the cavtratin group than in the control (AP) group in all three laminar layers. (C,D) RGC apoptosis decreased with application of cavtratin. RGCs were marked by immunostaining against Brn3a. TUNEL and Brn3a double labelled cells were quantified and the ratio of the double-labelled cell number to the total RGC number was used to evaluate apoptotic RGCs. (E,F) RGC survival increased in the model. RGCs were retrogradely labeled by injecting FG into the superior colliculus 7d before the acute ocular hypertension treatment. The FG labelled cells in the wholemount retinae were counted. Scale bar, 50 μm.