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. Author manuscript; available in PMC: 2008 Apr 15.
Published in final edited form as: Toxicol Appl Pharmacol. 2007 Jan 12;220(2):164–177. doi: 10.1016/j.taap.2006.12.035

FIG. 2.

FIG. 2

Effect on VE-cadherin localization and intercellular gap formation with As(III) exposure for 1 h. Confluent HAEC monolayers were either untreated (A) or treated with 1 μM As(III) (B), 5 μM As(III) (C) and 10 μM As(III) (D) for 1 h and the intercellular gaps (indicated with arrows) induced with As(III) treatment were visualized by immunofluorescence staining of VE-cadherin (green). The nuclei were stained with Hoechst (blue). Cleaved caspase-3 staining (green) for untreated (E) and 10 μM As(III) (F) treated cells is indicated by arrowheads. Pretreatment with 250 nM Gö 6976 for 1 h prior to and during 10 μM As(III) treatment (H) inhibited the As(III) induced gaps whereas 250 nM Gö 6976 only treatment (G) did not have any effect on the endothelial monolayer. Magnification=60X. The images are representative of 4 independent experiments performed.