Data from: Mechanical factors direct mouse aortic remodeling during early maturation

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.