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

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...

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Main Authors:	Laura Z. Vanags, PhD, Joanne T.M. Tan, PhD, Keyvan K. Galougahi, MD, PhD, Andreas Schaefer, MD, Steven G. Wise, PhD, Andrew Murphy, PhD, Ziad A. Ali, MD, PhD, Christina A. Bursill, PhD
Format:	Article
Language:	English
Published:	Elsevier 2018-04-01
Series:	JACC: Basic to Translational Science
Online Access:	http://www.sciencedirect.com/science/article/pii/S2452302X17302905

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spelling	doaj-d8d4a7812f1546ab8a5dc2f65548598b2020-11-24T23:14:31ZengElsevierJACC: Basic to Translational Science2452-302X2018-04-0132200209Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular PhenotypeLaura Z. Vanags, PhD0Joanne T.M. Tan, PhD1Keyvan K. Galougahi, MD, PhD2Andreas Schaefer, MD3Steven G. Wise, PhD4Andrew Murphy, PhD5Ziad A. Ali, MD, PhD6Christina A. Bursill, PhD7Immunobiology Group, The Heart Research Institute, Sydney, Australia; Sydney Medical School, University of Sydney, Sydney, AustraliaImmunobiology Group, The Heart Research Institute, Sydney, Australia; Sydney Medical School, University of Sydney, Sydney, AustraliaCenter for Interventional Vascular Therapy, Columbia University, New York, New York; Cardiovascular Research Foundation, New York, New YorkDepartment of Cardiology and Angiology, Hannover Medical School, Hannover, GermanyImmunobiology Group, The Heart Research Institute, Sydney, Australia; Sydney Medical School, University of Sydney, Sydney, AustraliaHaematopoiesis and Leukocyte Biology Group, Baker IDI Heart and Diabetes Institute, Melbourne, Australia; Department of Immunology, Monash University, Melbourne, AustraliaCenter for Interventional Vascular Therapy, Columbia University, New York, New York; Cardiovascular Research Foundation, New York, New YorkImmunobiology Group, The Heart Research Institute, Sydney, Australia; Sydney Medical School, University of Sydney, Sydney, Australia; Address for correspondence: Dr. Christina Bursill, Heart Health Theme, South Australia Health and Medical Research Institute, North Terrace, Adelaide, South Australia 5000, Australia.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. Key Words: apolipoprotein A-I, endothelialization, neointimal hyperplasia, platelet activation, stent biocompatibilityhttp://www.sciencedirect.com/science/article/pii/S2452302X17302905
collection	DOAJ
language	English
format	Article
sources	DOAJ
author	Laura Z. Vanags, PhD Joanne T.M. Tan, PhD Keyvan K. Galougahi, MD, PhD Andreas Schaefer, MD Steven G. Wise, PhD Andrew Murphy, PhD Ziad A. Ali, MD, PhD Christina A. Bursill, PhD
spellingShingle	Laura Z. Vanags, PhD Joanne T.M. Tan, PhD Keyvan K. Galougahi, MD, PhD Andreas Schaefer, MD Steven G. Wise, PhD Andrew Murphy, PhD Ziad A. Ali, MD, PhD Christina A. Bursill, PhD Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype JACC: Basic to Translational Science
author_facet	Laura Z. Vanags, PhD Joanne T.M. Tan, PhD Keyvan K. Galougahi, MD, PhD Andreas Schaefer, MD Steven G. Wise, PhD Andrew Murphy, PhD Ziad A. Ali, MD, PhD Christina A. Bursill, PhD
author_sort	Laura Z. Vanags, PhD
title	Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
title_short	Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
title_full	Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
title_fullStr	Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
title_full_unstemmed	Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype
title_sort	apolipoprotein a-i reduces in-stent restenosis and platelet activation and alters neointimal cellular phenotype
publisher	Elsevier
series	JACC: Basic to Translational Science
issn	2452-302X
publishDate	2018-04-01
description	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. Key Words: apolipoprotein A-I, endothelialization, neointimal hyperplasia, platelet activation, stent biocompatibility
url	http://www.sciencedirect.com/science/article/pii/S2452302X17302905
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Apolipoprotein A-I Reduces In-Stent Restenosis and Platelet Activation and Alters Neointimal Cellular Phenotype

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