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. Author manuscript; available in PMC: 2007 Jun 21.
Published in final edited form as: Neuroscience. 2006 Oct 30;143(3):779–792. doi: 10.1016/j.neuroscience.2006.08.079

Fig. 3.

Fig. 3

Time course of AQP4 expression changes after SCI. A) Quantitative analyses of immunoblotted AQP4 expression (Western blots) in uninjured and injured spinal cords (at the site of injury:T10) at different time points after SCI: 12h (n=5 for both sham and SCI), 24h (n=6 for both sham and SCI), 72h (n=5 for both sham and SCI), 7 d (n=5 for both sham and SCI); 14d (n=3 for both sham and SCI); 35 d (n= 12 for both sham and SCI); 40d (n=3 for sham and n=4 for SCI); 56d (n=4 for sham and n=5 for SCI) and 3.5 mo ( n=3 for sham and n=5 for SCI) and 9 mon (9m; n=6 for sham n=6 for SCI), shown as equidistant points on the X-axis. The Y-axis represents the relative intensity of the 30kD AQP4 band normalized to β-actin, and than to sham values (set to =1). AQP4 protein levels showed significant down-regulation in the first week after SCI, but robust and chronic up-regulation in the months after SCI (Bonferroni multiple comparisons tests; *=p<0.05). Representative AQP4 Western blots were shown above bar graphs for two sham samples (S1, S2) and two injured samples (I1, I2) for chronically injured spinal cords. B) Representative examples of AQP4 and GFAP Western blots 12h after SCI showed a significant increase in GFAP expression (∼50 kD), and no change for AQP4 expression in five injured samples (SCI) in T10. C) A representative example of AQP4 and GFAP Western blots 9 months after SCI show significant 4 fold increases in AQP4 expression (see Fig. 3A), and 1.4 fold increases in GFAP in injured T10. p<0.05. (Mean +/− SD).