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. 2021 Aug 12;11:16438. doi: 10.1038/s41598-021-96064-6

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© The Author(s) 2021

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 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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Aggravation of mSOD1 accumulation in the nerve by CCR2 ablation. (a) Immunostaining for mSOD1 in the sciatic nerves of CCR2-deficient SOD1^G93A mice and CCR2-positive littermates. (b) Accumulation of mSOD1 protein was significantly increased in CCR2-deficient SOD1^G93A mice than in CCR2-positive SOD1^G93A mice at 12 weeks of age (p = 0.032, n = 5). (c) Double immunostaining for mSOD1 and Schwann cells indicated a greater accumulation of mSOD1 protein in the sciatic nerves of CCR2-deficient SOD1^G93A mice showing an overflow of mSOD1 protein from Schwann cells and in the myelin sheath (arrows) compared with CCR2-positive SOD1^G93A mice at 12 weeks of age. (d) Immunostaining for mSOD1 protein in the lumbar spinal cord of CCR2-deficient SOD1^G93A mice and CCR2-positive littermates at 12 weeks of age. (e) There was no difference in the mSOD1⁺ area (%) between the two mouse genotypes at 12 weeks of age (p = 0.85, n = 6). The unpaired t test was used for statistical comparisons. Scale bars: (a) 20 μm; (c) 10 μm; (d) 100 μm. *p < 0.05. n.s. = not significant.