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Endothelial 2,6-Linked Sialic Acid Inhibits VCAM-1- Dependent Adhesion Under Flow Conditions¹

Yasunori Abe^*, C. Wayne Smith^*,, Julie P. Katkin, Lisa M. Thurmon^*, Xudong Xu, Leonardo H. Mendoza^* and Christie M. Ballantyne^2,*,§

^* Speros Martel Section of Leukocyte Biology, Department of Pediatrics, Department of Microbiology and Immunology, Pulmonary Medicine, Department of Pediatrics, and ^§ Section of Atherosclerosis, Department of Medicine, Baylor College of Medicine, Houston, TX 77030

We have previously shown that costimulation of endothelial cells with IL-1 + IL-4 markedly inhibits VCAM-1-dependent adhesion under flow conditions. We hypothesized that sialic acids on the costimulated cell surfaces may contribute to the inhibition. Northern blot analyses showed that Galß1-4GlcNAc 2,6-sialyltransferase (ST6N) mRNA was up-regulated in cultured HUVEC by IL-1 or IL-4 alone, but that the expression was enhanced by costimulation, whereas the level of Galß1-4GlcNAc/Galß1-3GalNAc 2,3-sialyltransferase (ST3ON) mRNA was unchanged. Removing both 2,6- and 2,3-linked sialic acids from IL-1 + IL-4-costimulated HUVEC by sialidase significantly increased VCAM-1-dependent adhesion, whereas removing 2,3-linked sialic acid alone had no effect; adenovirus-mediated overexpression of ST6N with costimulation almost abolished the adhesion, which was reversible by sialidase. The same treatments of IL-1-stimulated HUVEC had no effect. Lectin blotting showed that VCAM-1 is decorated with 2,6- but not 2,3-linked sialic acids. However, overexpression of 2,6-sialyltransferase did not increase 2,6-linked sialic acid on VCAM-1 but did increase 2,6-linked sialic acids on other proteins that remain to be identified. These results suggest that 2,6-linked sialic acids on a molecule(s) inducible by costimulation with IL-1 + IL-4 but not IL-1 alone down-regulates VCAM-1-dependent adhesion under flow conditions.

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