TY - JOUR
T1 - A fiber-based constitutive model predicts changes in amount and organization of matrix proteins with development and disease in the mouse aorta
AU - Cheng, Jeffrey K.
AU - Stoilov, Ivan
AU - Mecham, Robert P.
AU - Wagenseil, Jessica E.
N1 - Funding Information:
Acknowledgments This work was supported, in part, by the NIH [Grants RO1 HL074138 (RPM), R00 HL087563 (JEW), R01 HL105314 (RPM and JEW), and T32 HL007275 (JKC)].
PY - 2013/6
Y1 - 2013/6
N2 - 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.
AB - 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.
KW - Arterial mechanics
KW - Arteries
KW - Constitutive modeling
KW - Developmental remodeling
KW - Elastin
UR - http://www.scopus.com/inward/record.url?scp=84878738814&partnerID=8YFLogxK
U2 - 10.1007/s10237-012-0420-9
DO - 10.1007/s10237-012-0420-9
M3 - Article
C2 - 22790326
AN - SCOPUS:84878738814
SN - 1617-7959
VL - 12
SP - 497
EP - 510
JO - Biomechanics and Modeling in Mechanobiology
JF - Biomechanics and Modeling in Mechanobiology
IS - 3
ER -