Abstract 11205: Tropoelastin Inhibits Intimal Hyperplasia of Mouse Bioresorbable Arterial Vascular Grafts

Introduction: Neointimal hyperplasia, which results from the activation, proliferation and migration of vascular smooth muscle cells (SMCs), is a detrimental condition for vascular stents or vascular grafts that leads to stenosis. Preventing neointimal hyperplasia is critically important for the success of arterial vascular grafts. Hypothesis: We assessed the hypothesis that tropoelastin seeding will prevent SMC proliferation and neointimal hyperplasia in bioresorbable arterial vascular grafts. Methods: Poly (glycolic acid) (PGA) fiber mesh coated with poly (l-lactic-co- ε -caprolactone) (PLCL) scaffolds reinforced by poly (l-lactic acid) (PLA) nano-fibers were prepared as bioresorbable arterial grafts. Tropoelastin was then seeded onto the luminal surfaces of the grafts. Female C57BL/6 mice were randomly divided into 2 groups: 1. Tropoelastin seeded group (n=10), and 2. Unseeded group (n=10). The grafts were implanted as infra-renal aortic interposition conduits. Animals were followed for 8 weeks then sacrificed to evaluate neotissue formation. Results: Tropoelastin treatment substantially reduced the number of cells that stained positive for SMC (α-SMA) and Proliferating cell nuclear antigen (PCNA) in the vessel walls (Unseeded group: 60 ± 36/HPF vs. Tropoelastin seeded group: 21 ± 13/HPF, P =0.048, Unseeded group: 11.0 ± 5.6 /HPF vs. Tropoelastin seeded group: 4.8 ± 1.7/HPF, P =0.043, SMC and PCNA, respectively, HPF; high power field) (Fig. A, B). Tropoelastin significantly reduced the thickness of the intimal layer (Unseeded group: 91 ± 22 μm vs. Tropoelastin seeded group: 50 ± 11 μm, P =0.004) (Fig. C). Conclusions: Tropoelastin seeding is beneficial in preventing SMC proliferation and neointimal hyperplasia in bioresorbable arterial vascular grafts.