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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. 3 — Effects of astroglial IκKβ deletion on neuroinflammatory responses of the ocular hypertensive mouse retina. In order to determine the inflammatory status of retina (a) and optic nerve (b) tissues, cytokine titers were analyzed by ELISA. We detected significantly reduced production of pro-inflammatory cytokines in ocular hypertensive GFAP-IκKβ eyes compared to ocular hypertensive controls (IκKβ^f/f mice wild-type for cre). Bar graphs show fold decrease in ocular hypertension (OHT)-induced pro-inflammatory cytokine production with GFAP-IκKβ. Data (mean ± SD) from retina and optic nerve samples are presented by separate graphs (represents a minimum of 4 mice per group; **P < 0.001, *P < 0.05). c Isolated samples of retinal astroglia and microglia (by immunomagnetic cell selection) also presented reduced titers of TNF-α (a major pro-inflammatory cytokine relevant to glaucomatous neurodegeneration) in ocular hypertensive GFAP-IκKβ than ocular hypertensive IκKβ^f/f controls. However, there was no significant difference between the TNF-α titers in normotensive (NT) samples from GFAP-IκKβ or IκKβ^f/f mice (P > 0.05). Reduced production of TNF-α with GFAP-IκKβ was more significant in astroglia (**P < 0.001) than microglia (*P = 0.02). When the isolated samples of retinal Müller glia were similarly analyzed, no significant difference was detectable in the ocular hypertension-induced TNF-α production of Müller glia between GFAP-IκKβ mice and IκKβ^f/f controls (P = 0.06). d Astroglial pro-inflammatory phenotype was also studied by immunohistochemical analysis. Presented are TNF-α immunolabeling of retinal tissue sections (scale bar, 100 μm), and red or yellow boxed areas are shown in higher magnification. TNF-α immunolabeling (red) of GFAP+ astroglia (green) was prominently higher in ocular hypertensive IκKβ^f/f retina (white arrows) than normotensive controls. However, astroglial TNF-α immunolabeling was not detectable in the RGC layer (corresponding to astrocytes), but still detectable in the inner nuclear layer (corresponding to Müller glia; translucent arrows) of ocular hypertensive GFAP-IκKβ retinas. Blue indicates nuclear DAPI staining. RGCL, and INL mark retinal ganglion cells layer, and inner nuclear layer, respectively