Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype

• Published in: JACC. Basic to translational science 2018-04, Vol.3 (2), p.200-209
• Main Authors: Vanags, Laura Z., PhD, Tan, Joanne T.M., PhD, Galougahi, Keyvan K., MD, PhD, Schaefer, Andreas, MD, Wise, Steven G., PhD, Murphy, Andrew, PhD, Ali, Ziad A., MD, PhD, Bursill, Christina A., PhD
• Format: Article
• Language: English
• Subjects: apolipoprotein A-I; Cardiovascular; endothelialization; neointimal hyperplasia; platelet activation; PRECLINICAL RESEARCH; stent biocompatibility
• ISSN: 2452-302X; 2452-302X
• DOI: 10.1016/j.jacbts.2017.11.006

[Display omitted] •This study shows that apoA-I may be an alternative strategy to improve the biocompatibility of stents.•Systemic infusions of apoA-I reduce in-stent neointimal hyperplasia in a murine model of stenting.•The cellular phenotype of the neointima post-stenting is altered by apoA-I infusions such that the smooth muscle cell phenotype is preserved, and there are fewer macrophages.•There was an increase in endothelial cell content of the arteries post-stenting in the mice infused with apoA-I, indicating an enhancement of endothelialization.•Systemic infusions of apoA-I inhibit platelet activation. Even the most advanced drug-eluting stents evoke unresolved issues, including chronic inflammation, late thrombosis, and neoatherosclerosis. This highlights the need for novel strategies that improve stent biocompatibility. Our studies show that apolipoprotein A-I (apoA-I) reduces in-stent restenosis and platelet activation, and enhances endothelialization. These findings have therapeutic implications for improving stent biocompatibility.