Effect of adenylate cyclases activator on the cytoskeleton reorganization in thrombin-induced endothelial barrier dysfunction

This work executed on a model of endothelial monolayer in vitro, is devoted to the study of mechanisms leading to endothelial barrier dysfunction. The dysfunction inductor, thrombin, acts on endothelial cells through a specific receptor, triggering cascades of intracellular reactions (including cytoskeletal reorganization) resulting to increased of endothelial permeability. Thrombin-receptor interaction leads to dissociation of heterotrimeric G-protein subunits (Gi, Gq and G12/13), each of which is potentially capable to handle one or more possible ways of dysfunction development. In the present study we analyzed the role of Gi protein in the occurrence of cytoskeletal disturbances that lead to barrier dysfunction. According to our results, it can be assumed that the activity of Gi protein does not directly affect on the endothelial barrier properties