We have demonstrated that fibrin split product D-dimer (DD) hampers the incorporation of <$E nothing sup 14 roman C>-acetate into endothelial pericellular heparan sulfate (HS) and decreases HS binding to antithrombin. Fibrinogen fragment <$E gamma 117~-~133> is exposed in DD; hence, the binding of <$E gamma 117~-~133> fragment to the intercellular adhesion molecule-1 (ICAM-1) may be responsible for thte abovementioned DD effects. The <$E gamma 117~-~133> derived synthetic peptide gamma 3 revealed the same effect on the HS accumulation and properties, as DD did, whereas the scrambled control peptide was ineffective. Endothelial cell preincubation with the antibody, which blocks the ICAM-1 interaction with <$E gamma 117~-~133> fragment, abrogated DD- and gamma 3-induced alterations of the HS accumulation and properties. We suppose that ICAM-1 mediates the effect of DD concerning the down-regulation of the pericellular HS accumulation and its binding to antithrombin.

• Євдокимова Наталія Юріївна (біологічні науки)

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