4.5 Article

A fiber-based constitutive model predicts changes in amount and organization of matrix proteins with development and disease in the mouse aorta

期刊

BIOMECHANICS AND MODELING IN MECHANOBIOLOGY
卷 12, 期 3, 页码 497-510

出版社

SPRINGER HEIDELBERG
DOI: 10.1007/s10237-012-0420-9

关键词

Constitutive modeling; Elastin; Developmental remodeling; Arteries; Arterial mechanics

资金

  1. NIH [RO1 HL074138, R00 HL087563, R01 HL105314, T32 HL007275]

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Decreased elastin in mice (Eln+/-) yields a functioning vascular system with elevated blood pressure and increased arterial stiffness that is morphologically distinct from wild-type mice (WT). Yet, function is retained enough that there is no appreciable effect on life span and some mechanical properties are maintained constant. It is not understood how the mouse modifies the normal developmental process to produce a functioning vascular system despite a deficiency in elastin. To quantify changes in mechanical properties, we have applied a fiber-based constitutive model to mechanical data from the ascending aorta during postnatal development of WT and Eln+/- mice. Results indicate that the fiber-based constitutive model is capable of distinguishing elastin amounts and identifying trends during development. We observe an increase in predicted circumferential stress contribution from elastin with age, which correlates with increased elastin amounts from protein quantification data. The model also predicts changes in the unloaded collagen fiber orientation with age, which must be verified in future work. In Eln+/- mice, elastin amounts are decreased at each age, along with the predicted circumferential stress contribution of elastin. Collagen amounts in Eln+/- aorta are comparable to WT, but the predicted circumferential stress contribution of collagen is increased. This may be due to altered organization or structure of the collagen fibers. Relating quantifiable changes in arterial mechanics with changes in extracellular matrix (ECM) protein amounts will help in understanding developmental remodeling and in producing treatments for human diseases affecting ECM proteins.

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