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. 2010 Apr 12;207(4):881–896. doi: 10.1084/jem.20091258

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© 2010 Stockton et al.

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Figure 7. — Ccm2^+/− mouse endothelial cells exhibit increased pMLC in vivo and in vitro. (A) Endothelial cells isolated from Ccm2^+/+ and Ccm2^+/− mouse brain, lung, liver, and kidney were lysed and probed for CCM2 protein and pMLC content. 1, brain; 2, lung; 3, liver; 4, kidney. Endothelial cells from all organs have equivalent expression of CCM2 protein; however, Ccm2^+/− endothelial cells express 50% as much CCM2 as those from Ccm2^+/+ mice. Ccm2^+/− mouse endothelial cells exhibited increased pMLC content compared with WT. (B) Pulmonary endothelial cells were probed for pMLC and actin structure in vitro. Increased MLC phosphorylation and stress fiber content are seen in Ccm2^+/− cells. Bar, 50 µm. (C) Ccm2^+/− endothelial cells exhibit increased monolayer permeability reversible by treatment with ROCK inhibitor H-1152. Error bars are means ± SE (n = 6). *, P < 0.001; **, P < 0.05 compared with vehicle-treated Ccm2^+/+ cells.