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1 Cell Biology and Physiology, Washington University School of Medicine, St. Louis, MO, USA
2 Biomedical Engineering, Washington University, St. Louis, MO, USA
3 Mechanical Engineering, Washington University, St. Louis, MO, USA; Biomedical Engineering, Washington University, St. Louis, MO, USA
4 Program in Molecular Biology and Genetics, University of Utah, Salt Lake City, UT, USA
* To whom correspondence should be addressed. E-mail: bmecham{at}cellbiology.wustl.edu.
Supravalvular aortic stenosis (SVAS) is associated with decreased elastin and altered arterial mechanics. Mice with a single deletion in the elastin gene (ELN+/-) are models for SVAS. Previous studies have shown that elastin haploinsufficiency in these mice causes hypertension, decreased arterial compliance and changes in arterial wall structure. Despite these differences, ELN+/- mice have a normal lifespan, suggesting that the arteries remodel and adapt to the decreased amount of elastin. To test this hypothesis, we performed in vitro mechanical tests on abdominal aorta, ascending aorta and left common carotid arteries from ELN+/- and wildtype (C57BL/6J) mice. We compared the circumferential and longitudinal stress-stretch relationships and residual strains. The circumferential stress-stretch relationship is similar between genotypes and changes less than 3% with longitudinal stretch at lengths within 10% of the in vivo value. At mean arterial pressure, the circumferential stress in the ascending aorta is higher in ELN+/- than wildtype. Although arterial pressures are higher, the increased number of elastic lamellae in ELN+/- arteries results in similar tension/lamellae compared to wildtype. The longitudinal stress-stretch relationship is similar between genotypes for most arteries. Compared to wildtype, the in vivo longitudinal stretch is lower in ELN+/- abdominal and carotid arteries and the circumferential residual strain is higher in ELN+/- ascending aorta. The increased circumferential residual strain brings the transmural strain distribution in ELN+/- ascending aorta close to wildtype values. The mechanical behavior of ELN+/- arteries is likely due to the reduced elastin content combined with adaptive remodeling during vascular development.
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