In contrast, through effects on intracellular signalling, the cytoskeleton and junction-related molecules, Ang-1 reduces leakage from inflamed venules by restricting the number and size of gaps that form at endothelial cell junctions [80, 118, 119] . Ang-1 also suppresses expression of tissue factor induced by VEGF and tumour necrosis factor (TNF)-α, as well as expression of vascular cell adhesion molecule-1, intercellular adhesion molecule-1 and E-selectin. As a result, endothelial inflammation is suppressed [120] [121] [122] [123] .