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. 2022 Jul 19;79(8):431. doi: 10.1007/s00018-022-04461-5

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© The Author(s) 2022

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/.

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Fig. 5 — Surface P2X4 density is higher in macrophages of SOD1 as compared to WT mice before the onset and during the progression of the disease. A Western blotting of total and biotinylated surface proteins from peritoneal macrophages isolated from WT:WT (WT) and SOD1-G93A:WT (SOD1) mice at three time points (P40, P75 and P100). The anti-SOD1 antibody revealed 2 bands of different size corresponding to murine (m)SOD1 and human (h)SOD1-G93A confirming the genotype of the mouse. B Surface/total ratio shows that the number of surface P2X4 is increased in SOD1 macrophages as compared to WT at presymptomatic (P75) and symptomatic phase (P100). C Similar experiments from peritoneal macrophages isolated from WT:P2X4KI (P2X4KI) and SOD1:P2X4KI (SOD1KI) mice at the same 3 stages (P40, P75 and P100). D Surface/total ratio shows that the density of surface P2X4KI is similar between P2X4KI and SOD1:P2X4KI macrophages. (*p < 0.05, **p < 0.01, one-way ANOVA)