Mechanical factors direct mouse aortic remodelling during early maturation.

Autor:	Le VP; Department of Biomedical Engineering, Saint Louis University, St Louis, MO, USA., Cheng JK; Department of Biomedical Engineering, Washington University, St Louis, MO, USA., Kim J; Department of Mechanical Engineering and Materials Science, Washington University, St Louis, MO, USA., Staiculescu MC; Department of Mechanical Engineering and Materials Science, Washington University, St Louis, MO, USA., Ficker SW; Department of Biomedical Engineering, Saint Louis University, St Louis, MO, USA., Sheth SC; Department of Biomedical Engineering, Saint Louis University, St Louis, MO, USA., Bhayani SA; Department of Biomedical Engineering, Saint Louis University, St Louis, MO, USA., Mecham RP; Department of Cell Biology and Physiology, Washington University Medical School, St Louis, MO, USA., Yanagisawa H; Department of Molecular Biology, University of Texas Southwestern Medical Center, Dallas, TX, USA., Wagenseil JE; Department of Mechanical Engineering and Materials Science, Washington University, St Louis, MO, USA jessica.wagenseil@wustl.edu.
Jazyk:	angličtina
Zdroj:	Journal of the Royal Society, Interface [J R Soc Interface] 2015 Mar 06; Vol. 12 (104), pp. 20141350.
DOI:	10.1098/rsif.2014.1350
Abstrakt:	Numerous diseases have been linked to genetic mutations that lead to reduced amounts or disorganization of arterial elastic fibres. Previous work has shown that mice with reduced amounts of elastin (Eln+/-) are able to live a normal lifespan through cardiovascular adaptations, including changes in haemodynamic stresses, arterial geometry and arterial wall mechanics. It is not known if the timeline and presence of these adaptations are consistent in other mouse models of elastic fibre disease, such as those caused by the absence of fibulin-5 expression (Fbln5-/-). Adult Fbln5-/- mice have disorganized elastic fibres, decreased arterial compliance and high blood pressure. We examined mechanical behaviour of the aorta in Fbln5-/- mice through early maturation when the elastic fibres are being assembled. We found that the physiologic circumferential stretch, stress and modulus of Fbln5-/- aorta are maintained near wild-type levels. Constitutive modelling suggests that elastin contributions to the total stress are decreased, whereas collagen contributions are increased. Understanding how collagen fibre structure and mechanics compensate for defective elastic fibres to meet the mechanical requirements of the maturing aorta may help to better understand arterial remodelling in human elastinopathies. (© 2015 The Author(s) Published by the Royal Society. All rights reserved.)
Databáze:	MEDLINE
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