Abstract
The vascular endothelial solute barrier is formed by the regulated apposition of adherens and tight junctional proteins, and is controlled by several pharmacological and physiological mediators which govern junctional organization. We observe that barrier changes in vitro are associated with (1) the spatial redistribution of surface cadherins and occludin; (2) stabilisation of focal adhesive bonds; and (3) the progressive activation of matrix metalloproteinases. In response to peroxide, histamine and EDTA, endothelial cells sequester VE‐cadherin and alter its cytoskeletal binding. At the same time these mediators also enhance focal adhesion to the substratum. Lastly oxidants, cytokines and pharmacological mediators also trigger the activation of matrix metalloproteinases in a cytoskeleton and tyrosine phosphorylation dependent manner to degrade occludin, a tight junction element. These related in vitro phenomena may act cooperatively in inflammation to structurally stabilise cells during permeability, while remodelling cell junctions and substratum.Supported by grants HL47615, DK43785.
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