Monocyte adhesion to balloon-injured arteries: The influence of endothelial cell seeding

Abstract

Objective: Deendothelialization of injuries of the artery disrupts normal vascular homeostasis, affecting both the structural integrity of the blood vessel wall, as well as the interaction of the arterial surface with blood components such as platelets, leukocytes, and circulating proteins. Leukocyte and, in particular, monocyte recruitment to damaged vessels has been implicated in the pathogenesis of intimal hyperplasia. We hypothesize that reendothelialization is an important modulator of monocyte adhesion to healing arterial surfaces. Methods: New Zealand white rabbits (n = 20) were subjected to bilateral iliofemoral artery balloon injury. Cultured, autologous venous endothelial cells (ECs) were immediately seeded onto one vessel, whereas the contralateral artery received medium alone, to accelerate endothelial relining. Vessels were harvested (5-9 days after injury) for analysis of permeability (Evans Blue dye exclusion), endothelial coverage (anti-CD31 immunohistochemistry), monocyte adhesion (ex vivo binding of 51Na2CrO4-labeled monocytic THP-1 cells), and monocyte recruitment (RAM-11 immunohistochemistry). Results: Improved EC coverage was evidenced by positive staining for CD31 in the seeded vessels. Vessel wall permeability was markedly reduced in EC-seeded arteries (29% ± 10% vs 99% ± 0% surface Evans blue staining, P