This Article Full Text Full Text (PDF) Submit a response Alert me when this article is cited Alert me when eLetters are posted 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 McGillicuddy, C. J. Articles by Weinberg, P. D. Search for Related Content PubMed PubMed Citation Articles by McGillicuddy, C. J. Articles by Weinberg, P. D. Pubmed/NCBI databases Gene GEO Profiles HomoloGene UniGene Related Collections Animal models of human disease Pathophysiology Genetically altered mice

(Arteriosclerosis, Thrombosis, and Vascular Biology. 2001;21:1220.)
© 2001 American Heart Association, Inc.

Atherosclerosis and Lipoproteins

Distribution of Lipid Deposits Around Aortic Branches of Mice Lacking LDL Receptors and Apolipoprotein E

Christopher J. McGillicuddy; Martin J. Carrier; Peter D. Weinberg

From the School of Animal and Microbial Sciences (C.J.M., P.D.W.), University of Reading, Reading, UK, and the William Harvey Research Institute (M.J.C.), St Bartholomew’s and Royal London Hospital School of Medicine and Dentistry, London, UK.

Abstract—Mice with inactivated genes are increasingly used as models of human atherosclerosis. The aim of the present study was to determine whether the characteristic age-related distributions of lipid deposition seen around human arterial branches are replicated in such mice. Lesions occur downstream of branch ostia in immature human aortas, but these regions are spared in adult vessels, with lesions occurring more frequently at the sides or upstream of the branches. We determined the pattern of lipid staining around 102 intercostal branch ostia from apolipoprotein E/low density lipoprotein receptor double-knockout mice aged 9 to 20 weeks by using en face microscopy and a frequency-mapping technique. Lesion prevalence was high in the ostium and the region immediately surrounding it. Frequencies were 2.12±0.30 (mean±SEM, n=11) times higher upstream than downstream (P<0.01), but the pattern did not resemble the adult human pattern: there were no peaks in frequency at the sides or upstream of the branch, and there was no sparing downstream. Furthermore, a patch of sparing upstream of the branch was seen, which has not been reported for human vessels, and there was no trend toward a more upstream pattern with age. We conclude that knockout mice may not be a suitable model in which to investigate localizing factors.

Key Words: apolipoprotein E • LDL receptor • knockout mice • atherosclerosis • distribution

This article has been cited by other articles:

				A. Kazakidi, S.J. Sherwin, and P.D. Weinberg Effect of Reynolds number and flow division on patterns of haemodynamic wall shear stress near branch points in the descending thoracic aorta J R Soc Interface, June 6, 2009; 6(35): 539 - 548. [Abstract] [Full Text] [PDF]

				R. J. Petrovan, C. D. Kaplan, R. A. Reisfeld, and L. K. Curtiss DNA Vaccination Against VEGF Receptor 2 Reduces Atherosclerosis in LDL Receptor-Deficient Mice Arterioscler Thromb Vasc Biol, May 1, 2007; 27(5): 1095 - 1100. [Abstract] [Full Text] [PDF]

				J. Suo, D. E. Ferrara, D. Sorescu, R. E. Guldberg, W. R. Taylor, and D. P. Giddens Hemodynamic Shear Stresses in Mouse Aortas: Implications for Atherogenesis Arterioscler Thromb Vasc Biol, February 1, 2007; 27(2): 346 - 351. [Abstract] [Full Text] [PDF]

				D. E. Ferrara, D. Weiss, P. H. Carnell, R. P. Vito, D. Vega, X. Gao, S. Nie, and W. R. Taylor Quantitative 3D fluorescence technique for the analysis of en face preparations of arterial walls using quantum dot nanocrystals and two-photon excitation laser scanning microscopy Am J Physiol Regulatory Integrative Comp Physiol, January 1, 2006; 290(1): R114 - R123. [Abstract] [Full Text] [PDF]