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. 2018 Feb 21;15:53. doi: 10.1186/s12974-018-1093-9

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© The Author(s). 2018

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. 6 — Nrg-1 treatment positively modulates chemokine expression following SCI. a Analysis of chemokine expression in the spinal cord tissue was performed using real-time qPCR. There was a significant increase in the expression of pro-inflammatory chemokine CCL5, at 7-day post-injury, which was significantly reduced by Nrg-1 treatment. CCL5 mRNA level reached its maximum level at 42 days post-injury. However, no significant difference was found between vehicle- and Nrg-1-treated animals at this time-point. b Although the expression of CCL11, an immune modulatory chemokine, was not significantly changed at 3 and 7 days post-injury, it underwent a significant increase chronically at 42-day time-point. Nrg-1 treatment was able to significantly increase CCL11 expression compared to vehicle-treated group. c, d Expression of pro-inflammatory chemokines CXCL1 and CXCL2 was significantly elevated at 3-day post-injury. Nrg-1 treatment significantly reduced CXCL1 and CXCL2 expressions at this time-point. The overall tissue level of CXCL1 mRNA reached baseline levels at 7-day post-injury and remained stable until 42 days post-injury. CXCL2 expression, however, remained elevated at 7 and 42 days post-injury compared to uninjured group (significant 8.5-fold increase at 42-day). Nrg-1 treatment had no significant effect on CXCL2 expression at 7 and 42-day time-points. e Expression of the pro-inflammatory chemokine CXCL3was significantly upregulated 3 days after injury and reached its maximum levels chronically at 42 days post-SCI (p < 0.01). Nrg-1-treated animals showed a significant reduction in CXCL3 expression at 42-day time-point (31 times). f CXCL10 expression was not significantly changed following an injury at 3 and 7 days post-SCI, while it was significantly increased in the vehicle-treated group compared to un-injured animals at 42 days. Nrg-1 significantly decreased CXCL10 expression at this time-point (p < 0.001) (N = 4/group/time-point, *p < 0.05, **p < 0.01, ***p < 0.001, one-way ANOVA followed by Holm-Sidak post hoc test)