O16: TARGETING THE LOX-1 SCAVENGER RECEPTOR ATTENUATES ATHEROSCLEROSIS AND NEOINTIMAL HYPERPLASIA IN APO-E NULL TRANSGENIC MICE

Abstract Introduction The clinical consequences of atherosclerosis and post-procedure neointimal hyperplasia (NIH) represent a significant proportion the vascular surgeon's workload. Lectin-like oxidized low density lipoprotein receptor-1 (LOX-1) is class E scavenger receptor expressed in endothelial cells implicated NIH. This study aims to demonstrate therapeutic potential LOX-1 targeting using transgenic mouse model LOX-1-specific non-antibody synthetic protein scaffolds called affimers. Method Apolipoprotein-E (APO-E) null APO-E/LOX-1 double-null mice were fed high cholesterol western diet for 12 weeks. One group APO-E was treated subcutaneously with affimer. All underwent unilateral common femoral artery wire injury at week 8. Mice culled tissues harvested evaluation atherosclerotic burden Studies carried out Home Office approval. Result Compared controls, carotid bifurcation (p<0.05) total aortic plaque coverage (p<0.01) significantly reduced mice. Reductions observed affimer, however these non-significant. Femoral NIH by 16% double 11% affimer compared untreated reductions Conclusion demonstrates large vessel disease Knockout transgene produced promising results, while results following therapy less impressive. Improvements pharmacokinetics drug delivery optimisation are avenues future studies. Take-home message novel target large-vessel hyperplasia.