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. Author manuscript; available in PMC: 2017 Sep 1.
Published in final edited form as: Neurobiol Dis. 2016 May 1;93:226–242. doi: 10.1016/j.nbd.2016.04.010

Figure 5. Spinal cord injury-associated elevations in GFAP, vimentin and STAT3 signaling were reduced in PAR1 gene deficient mice.

Figure 5

Western blots and corresponding histograms show differential expression of GFAP, vimentin (VIM), pSTAT3 and STAT3 in the uninjured (C, Control) or injured PAR1+/+ or PAR1−/− spinal cord at 3 or 30 dpi. Protein samples isolated from the injury epicenter (E), above (A), or below (B) from PAR1+/+ or PAR1−/− mice were examined in parallel with uninjured samples in each case and results developed on the same film. SCI-induced elevations in GFAP, vimentin and pSTAT3 were all significantly reduced in mice lacking the PAR1 gene. In some cases, multiple bands for GFAP or vimentin were detected after SCI and the band used for quantification is shown at the arrowhead in each case. Histograms show the mean and standard error of ROD readings across multiple membranes (n = 3 to 4) normalized to Actin as loading control. (*P < 0.05, **P ≤ 0.01, ***P ≤ 0.001 NK).