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. 2017 Jun 27;14:130. doi: 10.1186/s12974-017-0905-7

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© The Author(s). 2017

Open AccessThis article is distributed under the terms of the Creative Commons Attribution 4.0 International License (http://creativecommons.org/licenses/by/4.0/), which permits unrestricted use, distribution, and reproduction in any medium, provided 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 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.

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Fig. 7 — Effect of ALF-186 treatment on retinal expression of Hsp90 mRNA and protein. a Fold induction of Hsp90 mRNA expression in ischemic retinal tissue compared to GAPDH in relation to the corresponding non-ischemic retinae analyzed by RT-PCR after ALF-186 and sGC inhibition (IRI vs. IRI + ALF-186, *** = p < 0.001; n = 8; data are mean ± SD). b, c Representative Western Blot image and densitometric analysis of n = 8 Western Blots showing the increase of retinal Hsp90 protein compared to β-Actin after ALF-186 (data are mean ± SD; IRI vs. IRI + ALF-186, *** = p < 0.001). This effect was not counteracted by ODQ. d Compared to IRI + PBS, Hsp90 protein expression is increased by ALF-186 treatment, mainly in RGC and bipolar cells. Quantification via frequency density of Hsp90 protein expression in both groups by histogram analysis revealed a significant increase of Hsp90 due to ALF-186 treatment (p < 0.001)