on January 4, 2007
Published online before print January 4, 2007, doi: 10.1161/01.ATV.0000257135.39571.5b
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Submitted on July 7, 2006
Accepted on December 19, 2006
Increased In-Stent Stenosis in ApoE Knockout Mice. Insights from a Novel Mouse Model of Balloon Angioplasty and Stenting
Ziad A. Ali ;
From the Department of Cardiovascular Medicine (Z.A.A., N.J.A., T.B., S.M., K.M.C.), University of Oxford, John Radcliffe Hospital, UK; Brivant Ltd (H.L., J.G.), Oranmore, Galway, Ireland; the Cardiovascular Research Group (N.A., M.W.), University of Sheffield, Northern General Hospital, UK; Sir William Dunn School of Pathology (D.R.G.), University of Oxford, UK; and the Department of Cardiological Sciences (Y.H.), St Georges Hospital Medical School, London, UK.
* To whom correspondence should be addressed. E-mail: keith.channon{at}cardiov.ox.ac.uk.
Objective--We aimed to develop and validate a model of angioplasty and stenting in mice that would allow investigation of the response to stent injury using genetically modified mouse strains.
Methods and Results--Aortic segments from either C57BL/6 wild-type or atherosclerotic ApoE-KO mice underwent balloon angioplasty alone or balloon angioplasty and stenting with a 1.25x2.5 mm stainless steel stent. Vessels were carotid-interposition grafted into genetically identical littermate recipients and harvested at 1, 7, 14, or 28 days. In wild-type mice, stenting generated an inflammatory vascular injury response between days 1 to 7, leading to the development of neointimal hyperplasia by day 14, which further increased in area by day 28 leading to the development of in-stent stenosis. Uninjured vessels and vessels injured by balloon angioplasty alone developed minimal neointimal hyperplasia. In stented ApoE-KO mice, neointimal area at 28 days was 30% greater compared with wild-type mice.
Conclusions--By reproducing important features of human stenting in atherosclerotic mice, we provide the potential to investigate molecular pathways and evaluate novel therapeutic targets for stent injury and restenosis.
Key words: vascular biology • genetically modified mice • angioplasty • stents • restenosis
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