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Am J Physiol Heart Circ Physiol 290: H1307-H1310, 2006. First published October 7, 2005; doi:10.1152/ajpheart.00196.2005
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Vascular injury response in mice is dependent on genetic background

Jürgen R. Sindermann,1,2,3 Christiane Köbbert,2,3 Adriane Skaletz-Rorowski,2,3 Günter Breithardt,2,3 Gabriele Plenz,2,3,4 and Keith L. March1

1Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indiana University Medical Center, Indianapolis, Indiana; 2Leibniz Institute for Arteriosclerosis Research; 3Department of Cardiology and Angiology; and 4Department of Thoracic and Cardiovascular Surgery, University of Münster, Münster, Germany

Submitted 28 February 2005 ; accepted in final form 14 September 2005

Mouse models are employed to unravel the pathophysiology of vascular restenosis. Although much effort has been spent on how to apply an adequate arterial injury, the influence of the genetic background of mice has not yet received sufficient consideration. The study presented herein was designed to demonstrate the influence of the mouse strain on vascular injury response. Mice of a defined background (50% 129 strain and 50% DBA strain) were backcrossed into either the 129 strain or the DBA strain. Male offspring were subjected to a femoral artery injury model by applying an electric current. Morphometric analysis revealed that backcrossing into the 129 strain resulted in a significant (P < 0.001) 17-fold increase in neointima formation (n = 17 mice) compared with backcrossing into the DBA strain (n = 19). The values of neointima area were 9.18 x 103 ± 2.13 x 103 and 0.54 x 103 ± 0.39 x 103 µm2, respectively. In conjunction, the vessel wall area was enhanced by 1.8-fold (P < 0.001). In contrast, no significant differences were found for the areas of the lumen and the tunica media. Similarly, a significant increase in neointima formation was also found for mice of pure 129 strain compared with pure DBA strain. The results underline the importance of the genetic background for studies on vascular injury response. Furthermore, because the mouse genome of the various strains is well defined, serial testing of the genetic background of mice will provide candidate genes and/or genetic modifiers controlling vascular injury response.

mouse strains; smooth muscle; neointima



Address for reprint requests and other correspondence: J. R. Sindermann, Dept. of Cardiology and Angiology, Univ. of Münster, Domagkstrasse 3, D-48149 Münster, Germany (e-mail: sinderm{at}uni-muenster.de)




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