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. 2018 May 24;9(6):626. doi: 10.1038/s41419-018-0682-y

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© The Author(s) 2018

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 license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license 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 license, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 2 — a Histogram of microtubule and vesicle-related protein fold changes in RA injured L4–L5 spinal cord segments with respect to sham-operated control obtained by analysis of proteomic data (upregulated in green; downregulated in red) obtained previously⁷. b Microphotographs of the ipsilateral spinal cord ventral horn from control (C) and RA-injured (RA) animals, showing immunostaining of KIF5C and DCTN1 with fluorescent Nissl counterstaining to reveal MNs at 7 dpi. Scale bar = 100 µm. c Western blot to quantify KIF5C and DCTN1 (n = 4; *p < 0.05 vs. control, ***p < 0.001 vs. control Student’s t-test). d Immunoblot and bar graph showing the analysis of EEA1, Sec31A, and p115 protein levels in L4 spinal cord segments (n = 4; *p < 0.05 vs. control, ***p < 0.001 vs. control Student’s t-test)