Fig. 7

CCL2 is expressed in both neurons and perineuronal cells in the DRG after injury. A–H Representative images of uninjured (A, C, E, G) and injured (B, D, F, H) DRGs stained for the co-translated RFP to localize CCL2 expression at 2 (B, D) and 3 (F, H) DPI. Very little CCL2 is present at baseline (A, C, E, G). CCL2 is rapidly upregulated in various perineuronal cells (arrowheads) in both the Flox control (B, F) and DCKO (D, H). Expression in neurons lags behind perineuronal expression in Flox controls (arrows, B, F), and little to no neuronal expression is seen in DCKOs (D, H). Large gray arrows indicate the likely meningeal expression. Scale bar is 50 μm. I–L Quantification of cells making CCL2 at 2 (I, K) and 3 (J, L) DPI in the cell body area of the DRGs. There is an apparent delayed onset of CCL2 expression in neurons (Flox Ax, I vs. J) when compared to perineuronal cells (K, L). The DCKOs show a strong CCL2 KO in neurons (I, J) and a trend toward fewer CCL2 expressing perineuronal cells (K, L). Individual images for the BIII-Tubulin and RFP channels are also displayed below each merged image (A–H). Data are the mean ± SEM, n = 5 for all groups except DCKO 2 DPI, where n = 4. One pair of 3 DPI Flox and one pair of 3 DPI DCKOs stained too badly to quantify and were excluded, and one 2 DPI DCKO Ax DRG was lost in sectioning. # Indicates a significant (p < 0.05) difference between Sh and Ax within a genotype and * indicates a significant difference between indicated genotypes within an injury condition (*p < 0.05, *** p < 0.001)