Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
Autor: | Andrew J. Murphy, Andreas Schaefer, Ziad A. Ali, Keyvan Karimi Galougahi, Laura Z. Vanags, Christina A. Bursill, Steven G. Wise, Joanne T.M. Tan |
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Jazyk: | angličtina |
Rok vydání: | 2018 |
Předmět: |
0301 basic medicine
Neointima lcsh:Diseases of the circulatory (Cardiovascular) system Apolipoprotein B CAD coronary artery disease HDL high-density lipoprotein apolipoprotein A-I PBS phosphate-buffered saline SMC smooth muscle cell PPAR peroxisome proliferator-activated receptor neointimal hyperplasia 030204 cardiovascular system & hematology Pharmacology stent biocompatibility endothelialization apoA-I apolipoprotein A-I rHDL reconstituted high- density lipoprotein 03 medical and health sciences PRECLINICAL RESEARCH 0302 clinical medicine Smooth muscle polycyclic compounds medicine platelet activation cardiovascular diseases Platelet activation Neointimal hyperplasia PCI percutaneous coronary intervention biology DES drug-eluting stent(s) business.industry nutritional and metabolic diseases equipment and supplies medicine.disease Cellular phenotype ABCA1 ATP-binding cassette transporter A1 Endothelial stem cell surgical procedures operative 030104 developmental biology lcsh:RC666-701 apoE−/− apolipoprotein E deficient biology.protein lipids (amino acids peptides and proteins) In stent restenosis Cardiology and Cardiovascular Medicine business |
Zdroj: | JACC: Basic to Translational Science JACC: Basic to Translational Science, Vol 3, Iss 2, Pp 200-209 (2018) |
ISSN: | 2452-302X |
Popis: | Visual Abstract Highlights • 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. Summary 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. |
Databáze: | OpenAIRE |
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