Author + information
- Received September 12, 2017
- Revision received October 20, 2017
- Accepted November 13, 2017
- Published online April 30, 2018.
- Laura Z. Vanags, PhDa,b,
- Joanne T.M. Tan, PhDa,b,
- Keyvan K. Galougahi, MD, PhDc,d,
- Andreas Schaefer, MDe,
- Steven G. Wise, PhDa,b,
- Andrew Murphy, PhDf,g,
- Ziad A. Ali, MD, PhDc,d and
- Christina A. Bursill, PhDa,b,∗ ()
- aImmunobiology Group, The Heart Research Institute, Sydney, Australia
- bSydney Medical School, University of Sydney, Sydney, Australia
- cCenter for Interventional Vascular Therapy, Columbia University, New York, New York
- dCardiovascular Research Foundation, New York, New York
- eDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, Germany
- fHaematopoiesis and Leukocyte Biology Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia
- gDepartment of Immunology, Monash University, Melbourne, Australia
- ↵∗Address for correspondence:
Dr. Christina Bursill, Heart Health Theme, South Australia Health and Medical Research Institute, North Terrace, Adelaide, South Australia 5000, Australia.
• 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.
This work was supported by a Heart Foundation of Australia PhD Scholarship (#PB 12S 6959 to Dr. Vanags) and a Heart Foundation of Australia Career Development Fellowship (#CR07S3331 to Dr. Bursill). The authors have reported that they have no relationships relevant to the contents of this paper to disclose.
All authors attest they are in compliance with human studies committees and animal welfare regulations of the authors’ institutions and Food and Drug Administration guidelines, including patient consent where appropriate. For more information, visit the JACC: Basic to Translational Science author instructions page.
- Received September 12, 2017.
- Revision received October 20, 2017.
- Accepted November 13, 2017.
- 2018 The Authors