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. Author manuscript; available in PMC: 2009 Jun 8.
Published in final edited form as: Lab Invest. 2007 Jun 18;87(8):807–817. doi: 10.1038/labinvest.3700595

Figure 5.

Figure 5

CXCL12-mediated restitution involves ROCK and MLCK. IEC-6 cells were wounded and restitution quantified by enumerating cells that migrated into the denuded ulcer in 3-5 fields of 2-3 wounds per experiment (n = 3 independent experiments). Wounded IEC-6 monolayers treated with 20 ng/ml CXCL12 demonstrated increased restitution relative to unstimulated cells (no stim). Treatment with the ROCK inhibitor Y27632 (10 μM) (a and b) or the MLCK inhibitor Drev-PIK (300 μM) (c and d) impeded CXCL12 restitution. Asterisks denote statistically significant difference from unstimulated monolayers (P ≤ 0.05).