Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy.

Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Research Abstract Details 

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Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Abstract Text:

W W Dye,R L Gleason,E Wilson,J D Humphrey,

Muscular dystrophy is characterized by skeletal muscle weakness and wasting, but little is known about possible alterations to the vasculature. Many muscular dystrophies are caused by a defective dystrophin-glycoprotein complex (DGC), which plays an important role in mechanotransduction and maintenance of structural integrity in muscle cells. The DGC is a group of membrane-associated proteins, including dystrophin and sarcoglycan-delta, that helps connect the cytoskeleton of muscle cells to the extracellular matrix. In this paper, mice lacking genes encoding dystrophin (mdx) or sarcoglycan-delta (sgcd-/-) were studied to detect possible alterations to vascular wall mechanics. Pressure-diameter and axial force-length tests were performed on common carotid arteries from mdx, sgcd-/-, and wild-type mice in active (basal) and passive smooth muscle states, and functional responses to three vasoactive compounds were determined at constant pressure and length. Apparent biomechanical differences included the following: mdx and sgcd-/- arteries had decreased distensibilities in pressure-diameter tests, with mdx arteries exhibiting elevated circumferential stresses, and mdx and sgcd-/- arteries generated elevated axial loads and stresses in axial force-length tests. Interestingly, however, mdx and sgcd-/- arteries also had significantly lower in vivo axial stretches than did the wild type. Accounting for this possible adaptation largely eliminated the apparent differences in circumferential and axial stiffness, thus suggesting that loss of DGC proteins may induce adaptive biomechanical changes that can maintain overall wall mechanics in response to normal loads. Nevertheless, there remains a need to understand better possible vascular adaptations in response to sustained altered loads in patients with muscular dystrophy.

Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Publishing Authors By Initials

WW Dye,RL Gleason,E Wilson,JD Humphrey,

For similar proteins: contractile proteins: muscle proteins: dystrophin-associated proteins: sarcoglycans research abstracts see: proteins: contractile proteins: muscle proteins: dystrophin-associated proteins: sarcoglycans research

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Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Journal Published:

PUBLICATION TYPE: Research Support, Non-U.S. Gov

Journal: Journal of applied physiology (Bethesda, Md. : 198

VOLUME: 103

Page Numbers: 664-72

Journal Abbreviation: J. Appl. Physiol.

ISSN: 8750-7587

DAY: 24

MONTH: 05

YEAR: 2007

Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Information

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LANGUAGE: eng

NlmUniqueID: 8502536

Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Keywords Mesh Terms:

KEYWORDS: Sarcoglycans

MESH TERMS: physiology

Chemical & Substance for Abstract: Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy. Information

Substance Name: Sarcoglycans

Registry Number: 0

Grant and Affiliation Information for Altered biomechanical properties of carotid arteries in two mouse models of muscular dystrophy.

AFFILIATION: Dept. of Biomedical Engineering, M. E. DeBakey Institute, Texas A&M University, College Station, TX 77843-3120, USA.

Country: United States

AGENCY: United States NHLBI

GRANT: HL-64372

ACRONYM: HL

MEDLINETA: J Appl Physiol

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