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. 2018 Mar 15;8:4641. doi: 10.1038/s41598-018-22848-y

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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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Ddit3 deficiency provides modest protection of RGCs after NMDA injury. (A) Representative images showing TUJ1 immunolabeled cells in the GCL of Ddit3 deficient (Ddit3^−/−), mice 7 days after intravitreal NMDA or PBS injection. Significant RGC loss occurred in wildtype (Ddit3^+/?), but Ddit3 deficient mice exhibited modest protection of RGCs after NMDA insult (n = 3 for PBS WT, n = 3 for NMDA WT, n = 8 for PBS Ddit3^−/−, n = 10 for NMDA Ddit3^−/−). (B) Quantification of TUJ1+ RGCs confirmed that Ddit3 deficient mice had significantly more surviving RGCs compared to wildtype mice 7d after NMDA injection (*p < 0.001 comparing PBS to NMDA; p = 0.8105 comparing WT to Ddit3^−/− NMDA; ns between genotypes). Scale bar: 50 μm.