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contributor authorBrankovic, Sonja A.
contributor authorHawthorne, Elizabeth A.
contributor authorYu, Xunjie
contributor authorZhang, Yanhang
contributor authorAssoian, Richard K.
date accessioned2019-09-18T09:07:14Z
date available2019-09-18T09:07:14Z
date copyright5/6/2019 12:00:00 AM
date issued2019
identifier issn0148-0731
identifier otherbio_141_08_081004
identifier urihttp://yetl.yabesh.ir/yetl1/handle/yetl/4259096
description abstractArterial stiffening is a hallmark of aging, but how aging affects the arterial response to pressure is still not completely understood, especially with regard to specific matrix metalloproteinases (MMPs). Here, we performed biaxial inflation–extension tests on C57BL/6 mice to study the effects of age and MMP12, a major arterial elastase, on arterial biomechanics. Aging from 2 to 24 months leads to both circumferential and axial stiffening with stretch, and these changes are associated with an increased wall thickness, a decreased inner radius–wall thickness ratio, and a decreased in vivo axial stretch. Analysis of in vivo stretch and stress–stretch curves with arteries from age- and sex-matched wild-type (WT) and MMP12-null arteries demonstrates that MMP12 deletion attenuates age-dependent arterial stiffening, mostly in the axial direction. MMP12 deletion also prevents the aging-associated decrease in the in vivo stretch and, in general, leads to an axial mechanics phenotype characteristic of much younger mice. Circumferential arterial mechanics were much less affected by deletion of MMP12. We conclude that the induction of MMP12 during aging preferentially promotes axial arterial stiffening.
publisherAmerican Society of Mechanical Engineers (ASME)
titleMMP12 Deletion Preferentially Attenuates Axial Stiffening of Aging Arteries
typeJournal Paper
journal volume141
journal issue8
journal titleJournal of Biomechanical Engineering
identifier doi10.1115/1.4043322
journal fristpage81004
journal lastpage081004-9
treeJournal of Biomechanical Engineering:;2019:;volume( 141 ):;issue: 008
contenttypeFulltext


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