Inflammatory mediators increase vascular permeability primarily by formation of intercellular
gaps between endothelial cells of post-capillary venules. Under these conditions …

Tight junctions (TJs) and adherens junctions (AJs) are dynamic structures linked to the actin
cytoskeleton, which control the paracellular permeability of epithelial and endothelial …

Fluid shear stress is an important mediator of vascular permeability, yet the molecular
mechanisms underlying the effect of shear on the blood-brain barrier (BBB) have yet to be …

Barrier stabilizing effects of cAMP as well as of the small GTPase Rac 1 are well established.
Moreover, it is generally believed that permeability‐increasing mediators such as thrombin …

Loss of endothelial barrier function is implicated in the etiology of metastasis,
atherosclerosis, sepsis and many other diseases. Studies suggest that sphingosine-1 …

Rho kinase (ROCK) is a downstream effector of Rho family GTPases, and two highly
homologous isoforms, ROCK1 and ROCK2, are similarly inhibited by the widely used …

It is well established that cAMP stabilizes endothelial barrier functions, in part by regulation
of VE-cadherin via EPAC/Rap 1. The aim of the present study was to investigate whether …

Bone contains a dense network of blood vessels that are essential to its homoeostasis,
endocrine function, mineral metabolism and regenerative functions. In addition, bone …

Cytotoxic necrotizing factor 1 (CNF1) is a bacterial virulence factor, the target of which is
represented by Rho GTPases, small proteins involved in a huge number of crucial cellular …

Objectives: To determine whether cyclic adenosine monophosphate (cAMP) is critically
involved in lipopolysaccharide (LPS)-induced breakdown of endothelial barrier functions in …