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Postnatal Time Course of Arterial Mechanics in a Mouse Model of Pathological Remodeling due to Decreased Elastin Amounts

[+] Author Affiliations
Jeffrey K. Cheng, Robert P. Mecham

Washington University, St. Louis, MO

Jessica E. Wagenseil

Saint Louis University, St. Louis, MO

Paper No. SBC2013-14346, pp. V01AT13A013; 2 pages
doi:10.1115/SBC2013-14346
From:
  • ASME 2013 Summer Bioengineering Conference
  • Volume 1A: Abdominal Aortic Aneurysms; Active and Reactive Soft Matter; Atherosclerosis; BioFluid Mechanics; Education; Biotransport Phenomena; Bone, Joint and Spine Mechanics; Brain Injury; Cardiac Mechanics; Cardiovascular Devices, Fluids and Imaging; Cartilage and Disc Mechanics; Cell and Tissue Engineering; Cerebral Aneurysms; Computational Biofluid Dynamics; Device Design, Human Dynamics, and Rehabilitation; Drug Delivery and Disease Treatment; Engineered Cellular Environments
  • Sunriver, Oregon, USA, June 26–29, 2013
  • Conference Sponsors: Bioengineering Division
  • ISBN: 978-0-7918-5560-7
  • Copyright © 2013 by ASME

abstract

Properly developed large elastic arteries serve as reservoirs that store stroke volume during systole and damp downstream blood pressure fluctuations. This function is enabled by the extracellular matrix (ECM) protein elastin. Mouse gene expression data reveals that elastin expression begins during embryonic development and peaks around postnatal day (P) 14. Expression then decreases to low levels for the remainder of adult life, indicating that elastin production during development is critical for a properly functioning vessel [1]. Reduced elastin in humans due to genetic mutations is associated with a congenital narrowing of the ascending aorta, known as supravalvular aortic stenosis, and chronic hypertension [2].

Copyright © 2013 by ASME

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