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. Author manuscript; available in PMC: 2017 Mar 2.
Published in final edited form as: Ther Deliv. 2012 Feb;3(2):263–276. doi: 10.4155/tde.11.151

Figure 6. Involvement of reactive oxygen species in the regulation of endothelial barrier function.

Figure 6

ROS derived from activated PMNs and endothelial cells in response to permeability enhancers (thrombin and VEGF) are involved in multiple signaling pathways leading to endothelial barrier disruption. Vascular ROS stimulate intracellular Ca2+, RhoA activity and phosphorylation of MLC, resulting in stress-fiber formation and increased contractility. ROS increase several kinase activities (e.g., p38 MAP kinase, protein kinase C and tyrosine kinase Pyk2) that are implicated in cytoskeletal remodeling and destabilization of intercellular junctions.

MLC: Myosin light chain; MMP: Matrix metalloproteinase; NOX: NADPH oxidase; PMN: Polymorphonuclear leukocyte; ROS: Reactive oxygen species; ZO: Zona occludens.