Skip to main content
. 2009 Oct 19;119(11):3437–3449. doi: 10.1172/JCI38476

Figure 6. APC downregulates SOD1 in spinal cord microvessels and blocks BSCB disruption in SOD1G93A mice.

Figure 6

(A and B) Immunoblotting (A) and densitometry (B) of human SOD1G93A and mouse mSOD1 in spinal cord microvessels isolated from SOD1G93A mice treated with 5A-APC or S360A-APC at 100 μg/kg/d i.p. for 4 weeks after disease onset. Relative band density was normalized to β-actin. n = 5 per group. (C) SOD1G93A and mSOD1 mRNA levels determined by QPCR in laser-captured microvessels from mice as in B. n = 5 per group. (D) Immunostaining for IgG (green) and endothelium (CD31, red) in the lumbar spinal cords of SOD1G93A mice treated with S360A-APC or 5A-APC as in B. Scale bar: 50 μm. (E) IgG signal intensity in the lumbar spinal cords of SOD1G93A mice treated as in B or with 40 μg/kg/d WT-APC. n = 5–8. (F) Hemosiderin deposits in the lumbar spinal cord of SOD1G93A mice treated as in B. Scale bar: 20 μm. (G) Quantification of lumbar spinal cord hemosiderin deposits in SOD1G93A mice from D and F. n = 5–8. (H) Relative abundance of ZO-1 and occludin, normalized to β-actin, from immunoblots of spinal cord microvessels isolated from SOD1G93A mice treated with 5A-APC as in B or with saline. n = 3–5. (E, G, and H) B6SJL denotes littermate controls.