Abstract
Occludin and zonular occludens (ZO)-1 in tight junctions (TJs) and actin play an important role in maintaining blood–brain barrier (BBB) endothelial ion and solute barriers. Malfunction of BBB by reactive oxygen species (ROS) has been attributed to the disruption of TJs. This study examined H 2O 2 effects on changes of paracellular permeability, actin, and TJ proteins (occludin and ZO-1) using primary culture of bovine brain microvessel endothelial cells. The BBB permeability, measured as transendothelial electrical resistance (TER), decreased in a dose- and time-dependent manner when treated with H 2O 2. Cytotoxicity test revealed that H 2O 2 did not cause cell death at 0.01, 0.1, and 1.0 mM H 2O 2. H 2O 2 caused increased protein expression of occludin (1.17- to 1.29-fold) and actin (1.2- to 1.3-fold). ZO-1 maintained steady state levels of expression. H 2O 2 caused rearrangement of occludin and ZO-1 at tight junctions and formation of actin stress fiber. Although ZO-1 did not show significant change in protein expression, permeability changes shown in the current study correlate with alterations in expression and localization of occludin, actin, and ZO-1. These data suggest that H 2O 2 induces increased paracellular permeability of BBB that is accompanied with redistribution of occludin and ZO-1 and increased protein expression of occludin and actin.
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