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

Laura Z Vanags; Joanne T M Tan; Keyvan K Galougahi; Andreas Schaefer; Steven G Wise; Andrew Murphy; Ziad A Ali; Christina A Bursill

doi:10.1016/j.jacbts.2017.11.006

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

JACC Basic Transl Sci. 2018 May 30;3(2):200-209. doi: 10.1016/j.jacbts.2017.11.006. eCollection 2018 Apr.

Authors

Laura Z Vanags^{1

2}, Joanne T M Tan^{1

2}, Keyvan K Galougahi^{3

4}, Andreas Schaefer⁵, Steven G Wise^{1

2}, Andrew Murphy^{6

7}, Ziad A Ali^{3

4}, Christina A Bursill^{1

2}

Affiliations

¹ Immunobiology Group, The Heart Research Institute, Sydney, Australia.
² Sydney Medical School, University of Sydney, Sydney, Australia.
³ Center for Interventional Vascular Therapy, Columbia University, New York, New York.
⁴ Cardiovascular Research Foundation, New York, New York.
⁵ Department of Cardiology and Angiology, Hannover Medical School, Hannover, Germany.
⁶ Haematopoiesis and Leukocyte Biology Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia.
⁷ Department of Immunology, Monash University, Melbourne, Australia.

Abstract

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.

Keywords: ABCA1, ATP-binding cassette transporter A1; CAD, coronary artery disease; DES, drug-eluting stent(s); HDL, high-density lipoprotein; PBS, phosphate-buffered saline; PCI, percutaneous coronary intervention; PPAR, peroxisome proliferator-activated receptor; SMC, smooth muscle cell; apoA-I, apolipoprotein A-I; apoE−/−, apolipoprotein E deficient; apolipoprotein A-I; endothelialization; neointimal hyperplasia; platelet activation; rHDL, reconstituted high- density lipoprotein; stent biocompatibility.