Fig. 7: Activation of the CCR2 pathway in ALS patients and in the hTDP-43Tg/Tg mice across different disease stages.
From: The CCL2-CCR2 axis drives neuromuscular denervation in amyotrophic lateral sclerosis
A–C CCR2 staining in the GC muscle of wild-type (WT; A) and late symptomatic (postnatal day 19) hTDP-43Tg/Tg mice (Tg/Tg; B, C). C High magnification image reveals co-expression of CCR2 and CD45 markers, however, not all of the CD45+ cells show CCR2 staining. D–F Quantitative analysis of CCR2+ cells in the GC muscle of presymptomatic (D), early symptomatic (E) and late symptomatic (F) hTDP-43Tg/Tg mice. G–H CCR2 staining in the skeletal muscle of control individuals (control; G) and ALS patients (ALS; H). I Quantification of CCR2+ cells in the skeletal muscle of healthy control (CTRL-2 in Table 1) and ALS patient (ALS-1 in Table 1) muscle samples. Data is presented as mean ± sem. Scale bar represents 50 µm on (A, B), 20 µm on (C) and 40 µm on (G, H). Data analysis: (D) Presymptomatic stage: n = 4 (WT), n = 3 (Tg/Tg), unpaired, two-tailed t-test; (E) Early symptomatic stage: n = 3 (WT, Tg/Tg), unpaired, two-tailed t-test, p = 0.0234; (F) Late symptomatic stage: n = 4 (WT, Tg/Tg), unpaired, two-tailed t-test, p = 0.0012; (I) Human muscle samples: n = 4 (control, ALS), unpaired, two-tailed t-test, p = 0.0038. * = p < 0.05; ** = p < 0.01.
