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. Author manuscript; available in PMC: 2012 Apr 1.
Published in final edited form as: Exp Cell Res. 2010 Nov 25;317(6):859–872. doi: 10.1016/j.yexcr.2010.11.011

Figure 3. Effect of p190RhoGAP inhibition on OxPAPC-mediated protection against thrombin-induced EC barrier dysfunction.

Figure 3

Figure 3

Figure 3

A – C: HPAEC were transfected with p190RhoGAP -specific siRNA or non-specific RNA duplexes for 72 hr. A - EC were treated with OxPAPC (10 μg/ml, 15 min) or left untreated prior to thrombin (0.1 U/ml) challenge, and TER was monitored over the time. B and C - EC were subjected to thrombin challenge (0.1 U/ml, 15 min) with or without OxPAPC pretreatment (10 μg/ml, 15 min). Analysis of actin cytoskeletal remodeling was performed by immunofluorescence staining with Texas Red phalloidin. Paracellular gaps are marked by arrows. Bar graphs represent quantitative analysis of gap formation in control and treated HPAEC. Data are expressed as mean ± SD of three independent experiments; *p<0.05. (B). Phosphorylation status of MYPT1 or MLC was determined by western blot with specific antibodies. Equal protein loading was confirmed by re-probing of membranes with antibody to housekeeping protein β-tubulin. P190RhoGAP depletion was confirmed by probing of membranes with specific antibody (C). Result of densitometry shown as mean ± SD, * p<0.05