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. 2011 Mar 15;22(6):795–805. doi: 10.1091/mbc.E10-06-0505

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© 2011 Farber et al. This article is distributed by The American Society for Cell Biology under license from the author(s). Two months after publication it is available to the public under an Attribution–Noncommercial–Share Alike 3.0 Unported Creative Commons License (http://creativecommons.org/licenses/by-nc-sa/3.0).

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FIGURE 4: — Transient knockdown of Shrm2 regulates endothelial migration. (A) siControl, siShrm2, or untreated cells with Y27632 were subjected to a scratch wound assay and were stained with phalloidin at 1, 12, and 24 h postscratch. (B) Quantification of a scratch wound assay from live C166 cells treated with siControl or siShrm2, represented by the mean percentage of wound closure ± SD (n = 5). (C) Migration of siControl and siShrm2 C166 cells in the presence or absence of Y27632 was assessed with a Boyden chamber. (D) Migration of siControl and siShrm2-treated HUVEC cells in a Boyden chamber. The number of migrated nuclei is represented by the mean ± SEM (n = 6) in C and D. (E) Untreated C166 cells were scratch wounded and stained for Shrm2 and actin at 2, 12, and 24 h postscratch. Asterisks indicate cells that have detached from the epithelial sheet and have lost Shrm2 expression. (F and G) At 2 h after scratch wounding C166 cells, Rock1 localizes to the leading edge of siControl (F) but not siShrm2 (G) C166 cells. Immunostaining for β-catenin (Ei and Fi). Scale bars = 100 μm in A; 25 μm in B, E, and F.