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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 8. Spinal cord injury-induced elevations in markers of astrogliosis and apoptosis were reduced in mice lacking the PAR1 gene.

Figure 8

Histograms show transcriptional changes in RNA encoding GFAP (A, B), vimentin (VIM, (C, D)), neurocan (NCAN, (E, F)), and BIM (G, H) in the spinal cord of PAR1+/+ or PAR1−/− uninjured controls (C), or in the 3 mm of spinal cord surrounding the injury epicenter (E), or that above (A), or below (B), at 7 and 30 dpi. The RNA expression levels shown are expressed as a percent of the uninjured genotype control and these data were used for statistical comparisons. In addition, to facilitate interpretation of any impact of PAR1 gene deletion on gene expression in the uninjured spinal cord, and to permit statistical comparisons, expression levels shown for uninjured control PAR1−/− mice are expressed as a percent of uninjured PAR1+/+ controls. Baseline levels of GFAP, neurocan and BIM were higher in PAR1−/− compared to PAR1+/+ mice. (*P < 0.05, **P ≤ 0.01, ***P ≤ 0.001 NK).