Summary
Glycosaminoglycans (GAGs) are an important component of endothelial barrier function.
Early passage human umbilical vein endothelial cells were grown to confluence on transparent
micropore filters and barrier function assessed as transendothelial electrical resistance
(TEER) and permeability to albumin and sucrose. Unfractionated heparin and the LMW
heparin Clexane decreased endothelial permeability to both sucrose and albumin and
increased TEER. Chondroitin 6-sulphate also augmented barrier function, but other
GAGs had no effect. Interleukin-1 increased permeability to albumin and sucrose and
decreased TEER. Although heparin attenuated the effect of IL-1 on TEER and sucrose
permeability, it could not restore the barrier to albumin transfer. Denuded endothelial
matrix presented a negligible barrier, which was not enhanced by heparin. When sulphation
of endogenous GAGs was inhibited by chlorate, barrier function was compromised and
was not restored by exogenous heparin. Thus heparin enhances the barrier function
of resting endothelium, but cannot completely overcome the increased permeability
resulting from exposure to IL-1 or substitute for endogenous GAGs.
