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
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