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Fig. 4 | Journal of Neuroinflammation

Fig. 4

From: A novel interaction between CX3CR1 and CCR2 signalling in monocytes constitutes an underlying mechanism for persistent vincristine-induced pain

Fig. 4

CX3CR1 deficiency increases CCR2 expression in vivo. a Representative blot for CCL2 (15 kDa) in CX3CR1+/GFP and CX3CR1GFP/GFP sciatic nerves. b Quantification of CCL2 band density normalised to α-tubulin (mean ± SEM, n = 3). Basal expression of CCL2 in sciatic nerve homogenates is significantly higher in CX3CR1-deficient mice relative to saline-treated CX3CR1 heterozygous. VCR significantly increases CCL2 in both genotypes. *p < 0.05, ***p < 0.005, one-way ANOVA, Tukey’s test. c Representative images of GFP (macrophages) and CCL2 (red) in sciatic nerve transverse sections at day 11. Scale bar = 50 μm. d Quantification of the percentage of GFP+ profiles that are also CCL2+. Two cycles of VCR significantly increases the percentage of GFP+/CCL2+ macrophages in both genotypes (mean ± SEM, n = 4 mice per group). ***p < 0.005, one-way ANOVA, post hoc Tukey’s test. e Representative dot blots for peritoneal lavages. Numbers in the gates refer to percentage of positive cells. f Bar chart representing number of F4/80Ly6C+CCR2+ events (mean ± SEM, n = 3). *p < 0.05, **p < 0.01 and ***p < 0.005, one-way ANOVA, Tukey’s test

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