Arg-Glu-Asp-Val Peptide Immobilized on an Acellular Graft Surface Inhibits Platelet Adhesion and Fibrin Clot Deposition in a Peptide Density-Dependent Manner

Acellular blood vessels possess high potential to be used as tissue-engineered vascular scaffolds. Previously, a high patency was achieved for an Arg-Glu-Asp-Val (REDV) peptide-immobilized small-diameter acellular graft in a minipig model. Results revealed the potential of the peptide to capture a circulating cell and also to suppress fibrin clot deposition. Here, the effect of REDV peptide density on the blood response under ex vivo blood perfusion conditions was investigated. When endothelial cells or platelets were seeded under static conditions, the number of adherent endothelial cells increased with the increase in peptide density. Platelets scarcely adhered on the surface where the peptide density was above 18.9 × 10^–4 molecules per nm³. Fibrin clot deposition and circulating cell capture were evaluated in a minipig extracorporeal circulatory system. The fibrin clot did not form on the peptide-immobilized surface, in the range of peptide modification density that was evaluated, whereas the unmodified surface was covered with microthrombi. REDV-specific blood circulating cells were captured on the peptide-immobilized surface with a density above 18.9 × 10^–4 molecules per nm³. These results illustrated, under ex vivo blood perfusion conditions, that the REDV-immobilized acellular surface was able to capture cells and also suppress platelet adhesion and fibrin clot deposition in a peptide density-dependent manner.