SEARCH

SEARCH BY CITATION

Additional supporting information available online.

FilenameFormatSizeDescription
STEM_577_sm_suppinfoFig1.tif459KSupplementary Fig. 1. Western blot analysis of ROCK, Rac1 and PI3K inhibition on the activation of Akt at 24hrs. (A) Lysates derived from NPCs treated with Y27632 (Y), Rac1 inhibitor and LY294002 (LY) were assessed by Western blotting for phosphorylated and total levels of Akt. (B) Densitometric analysis comparing the ratio of phosphorylated Akt to total Akt. Mean ± SEM of n=3 independent experiments. **P<0.01; ***P<0.001.
STEM_577_sm_suppinfoFig2.tif474KSupplementary Fig. 2. Western blot analysis of ROCK, Rac1 and PI3K inhibition on the activation of myosin light chain II at 24hrs. (A) Lysates derived from NPCs treated with Y27632 (Y), Rac1 inhibitor and LY294002 (LY) were assessed by Western blotting for phosphorylated and total levels of myosin light chain II (MLCII). (B) Densitometric analysis comparing the ratio of phosphorylated MLCII to total MLCII. Mean ± SEM of n=3 independent experiments. **P<0.01; ***P<0.001.
STEM_577_sm_suppinfoFig3.tif1157KSupp. Fig. 3. Effect of ROCK inhibition at the cortical injury site. (A, C, D) Infusion of BrdU+/-Y27632 into the lateral ventricle produced a stab injury in the right cortex (right of panel A). Immunohistochemistry for BrdU (red) and GFAP (green), showed numerous BrdU+ and GFAP+ cells, especially in the area close to the margin of the injury at 1 week. White arrow in (A) indicates midline. LV, lateral ventricle; IS injury site. Scale bars; (A) 200μm, (C, D) 50μm. ROCK inhibition did not affect the total number of BrdU+ cells at (B) the injury periphery (represented by boxes 1-4 in panel A) or the injury margin (represented by columns in panel A). (E) ROCK inhibition increased the percentage of proliferative astrocytes at the injury margin but had no effect on CD11b+ macrophages. Mean ± SEM of 5 treated mice and 4 control mice. *P<0.05.
STEM_577_sm_suppinfo.doc58KSupporting Information

Please note: Wiley Blackwell is not responsible for the content or functionality of any supporting information supplied by the authors. Any queries (other than missing content) should be directed to the corresponding author for the article.