This Article Full Text Full Text (PDF) All Versions of this Article: 27/4/714    most recent 01.ATV.0000261873.86623.e1v1 Alert me when this article is cited Alert me if a correction is posted Citation Map Services Email this article to a friend Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Request Permissions Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Jackson, C. L. Articles by Krams, R. Search for Related Content PubMed PubMed Citation Articles by Jackson, C. L. Articles by Krams, R. Related Collections Related Article

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2007;27:714.)
© 2007 American Heart Association, Inc.

Brief Reviews

Assessment of Unstable Atherosclerosis in Mice

Christopher L. Jackson; Martin R. Bennett; Erik A.L. Biessen; Jason L. Johnson; Rob Krams

From the Bristol Heart Institute (C.L.J., J.L.J.), University of Bristol, UK; the University of Cambridge (M.R.B.), UK; the University of Leiden (E.A.L.B.), The Netherlands; and Laboratory of Physiology (R.K.), Free University Amsterdam, The Netherlands.

Correspondence to Christopher L. Jackson, Bristol Heart Institute, Level 7, Bristol Royal Infirmary, Bristol, UK. E-mail chris.jackson{at}bristol.ac.uk

There is an urgent need for representative animal models where prospective examination of the events leading up to plaque rupture and the rupture process itself can be performed. Recently, reports have begun to emerge that apolipoprotein E and low density lipoprotein receptor knockout mice may spontaneously develop unstable atherosclerosis, with plaques in certain parts of the arterial tree showing features suggestive of plaque rupture. Here we discuss the problems inherent in applying definitions of plaque rupture as seen in human arteries to mice; the anatomic locations in mice where unstable plaques do and do not occur; methods of inducing plaque instability in mice; and how to assess plaque stability in mice. These considerations lead us to a number of general recommendations.

There is an urgent need for representative animal models where prospective examination of the events leading up to plaque rupture and the rupture process itself can be performed. Recently, reports have begun to emerge that apolipoprotein E and low density lipoprotein receptor knockout mice may spontaneously develop unstable atherosclerosis, with plaques in certain parts of the arterial tree showing features suggestive of plaque rupture. Here we discuss the problems inherent in applying definitions of plaque rupture as seen in human arteries to mice; the anatomic locations in mice where unstable plaques do and do not occur; methods of inducing plaque instability in mice; and how to assess plaque stability in mice. These considerations lead us to a number of general recommendations.

Key Words: plaque rupture • animal models • apoE knockout mouse • vascular histopathology

Related Article:

Two Views on Plaque Rupture

Göran K. Hansson and Donald D. Heistad
Arterioscler. Thromb. Vasc. Biol. 2007 27: 697. [Full Text] [PDF]

This article has been cited by other articles:

				F. Johansson, F. Kramer, S. Barnhart, J. E. Kanter, T. Vaisar, R. D. Merrill, L. Geng, K. Oka, L. Chan, A. Chait, et al. Type 1 diabetes promotes disruption of advanced atherosclerotic lesions in LDL receptor-deficient mice PNAS, February 12, 2008; 105(6): 2082 - 2087. [Abstract] [Full Text] [PDF]

				J. F. Bentzon, C. S. Sondergaard, M. Kassem, and E. Falk Smooth Muscle Cells Healing Atherosclerotic Plaque Disruptions Are of Local, Not Blood, Origin in Apolipoprotein E Knockout Mice Circulation, October 30, 2007; 116(18): 2053 - 2061. [Abstract] [Full Text] [PDF]

				G. K. Hansson and D. D. Heistad Two Views on Plaque Rupture Arterioscler. Thromb. Vasc. Biol., April 1, 2007; 27(4): 697 - 697. [Full Text] [PDF]

				E. Falk, S. M. Schwartz, Z. S. Galis, and M. E. Rosenfeld Putative Murine Models of Plaque Rupture Arterioscler. Thromb. Vasc. Biol., April 1, 2007; 27(4): 969 - 972. [Full Text] [PDF]