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1 Department of Cardiology and Angiology, University of Munster, Munster, Germany; Leibniz Institute for Arteriosclerosis Research, University of Munster, Munster, Germany; Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indiana University Medical Center, Indianapolis, IN, USA
2 Leibniz Institute for Arteriosclerosis Research, University of Munster, Munster, Germany; Department of Cardiology and Angiology, University of Munster, Munster, Germany
3 Department of Cardiology and Angiology, University of Munster, Munster, Germany; Leibniz Institute for Arteriosclerosis Research, University of Munster, Munster, Germany
4 Leibniz Institute for Arteriosclerosis Research, University of Munster, Munster, Germany; Department of Cardiology and Angiology, University of Munster, Munster, Germany; Department of Thoracic and Cardiovascular Surgery, University of Munster, Munster, Germany
5 Krannert Institute of Cardiology and Indiana Center for Vascular Biology and Medicine, Indiana University Medical Center, Indianapolis, IN, USA
* To whom correspondence should be addressed. E-mail: sinderm{at}uni-muenster.de.
Mouse models are employed to unravel the pathophysiology of vascular restenosis. Although much efforts have 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 herein presented study was designed to demonstrate the influence of the mouse strain on vascular injury response. Mice of a defined background (50% 129 strain / 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 µm2 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, since 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.
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