title: Wall properties of the apolipoprotein E-deficient mouse aorta.
abstract: OBJECTIVE
  We quantified the dysfunction of the aortic wall, determined structural and elastic properties, and provided histological data of the thoracic aortas of apolipoprotein E (apoE)-deficient mice which are used as model of atherosclerosis.
  
  
  METHODS
  Six young 10-12 week-old (apoE)-deficient mice of both sexes were studied and six age-matched C57BL/6J wild-type mice were used as control group. We performed extension-inflation mechanical tests at three different axial stretches (λ(z) = 1.6, 1.8, and 2.0), under maximally contracted or totally relaxed state of the vascular smooth muscle cells. Classical histology was performed to the arterial segments.
  
  
  RESULTS
  Control aortas were generally more distensible than the (apoE)-deficient mouse aortas under both relaxed and contracted smooth muscle. Also, aortas from (apoE)-deficient mice were stiffer (higher incremental elastic modulus) than control aortas. Control aortas exhibited a higher active diameter response compared to (apoE)-deficient mouse aortas, despite the fact that vascular smooth muscle cell density was increased by approximately 15% in the (apoE)-deficient mouse aortas.
  
  
  CONCLUSIONS
  We found substantial changes in the structural and elastic properties of the wall, in the active diameter response and in the histology of (apoE)-deficient mouse aortas compared to the control group. Our data can be used in the development of constituent-based models of the arterial wall and in studying the changes in arterial wall properties in presence of disease, such as atherosclerosis.
authors: Laboratory of Hemodynamics and Cardiovascular Technology, Institute of Bioengineering, Ecole Polytechnique Fédérale de Lausanne, BM 5128 (Bâtiment BM), Station 17, 1015 Lausanne, Switzerland. aristotelis.agianniotis@epfl.ch
authors: Aristotelis
authors: A
authors: Agianniotis
authors: Nikos
authors: N
authors: Stergiopulos
mesh_terms: D000818:Animals; D001013:Aorta, Thoracic / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology; D001018:Aortic Diseases / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D001057:Apolipoproteins E / Q000172:deficiency* / Q000235:genetics; D050197:Atherosclerosis / Q000235:genetics / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D001696:Biomechanical Phenomena; D003187:Compliance; D004195:Disease Models, Animal; D055119:Elastic Modulus; D005260:Female; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D018345:Mice, Knockout; D009131:Muscle, Smooth, Vascular / Q000378:metabolism / Q000473:pathology / Q000503:physiopathology*; D011312:Pressure; D059289:Vascular Stiffness; D014661:Vasoconstriction; D014664:Vasodilation
chemical_list: D001057:Apolipoproteins E