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. 2020 Aug 28;17:252. doi: 10.1186/s12974-020-01930-1

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© The Author(s) 2020

Open AccessThis 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 licence, and indicate if changes were made. The images or other third party material in this article are included in the article's Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article's Creative Commons licence 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 licence, visit http://creativecommons.org/licenses/by/4.0/. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated in a credit line to the data.

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Fig. 5 — Transgenic effects on RGC counts. a Composite images of the whole-mounted retinas immunolabeled for RPBMS, an RGC marker. Red boxed areas are shown in higher magnification (scale bar, 100 μm). Ocular hypertensive control eyes (IκKβ^f/f mice wild-type for cre) exhibited a visible loss of RPBMS-labeled RGC somas compared to normotensives; however, RGC bodies were well protected in ocular hypertensive eyes of GFAP-IκKβ mice. RPBMS-labeled RGC somas were counted and the neuron loss was determined in ocular hypertensive eyes after adjusting to normotensive fellow eyes. The number of RPBMS-labeled RGCs was significantly higher in ocular hypertensive GFAP-IκKβ retinas than ocular hypertensive IκKβ^f/f controls (***P < 0.001). Bar graphs in panel b present RGC counts in GFAP-IκKβ mice and IκKβ^f/f controls with or without experimentally induced ocular hypertension, and bar graphs in panel c show percentage of RGC loss in ocular hypertensive transgenic or control animals. Presented data (mean ± SD) represents a minimum of 16 mice per group. Transgenic deletion of astroglial IκKβ resulted in an approximately 63% protection of RGC somas in ocular hypertensive eyes