Thrombin-cleaved syndecan-3/-4 ectodomain fragments mediate endothelial barrier dysfunction.

We suggest that thrombin can cleave syndecan-3/4 ectodomain into fragments which interact with endothelial cells causing paracellular hyperpermeability. This may have important implications in the pathogenesis of vascular dysfunction during sepsis or thrombotic disease states where thrombin is activated.