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Effect of Boundary Stiffness on Contractility Profile of Valvular Interstitial Cells

[+] Author Affiliations
Mehmet H. Kural

Worcester Polytechnic Institute, Worcester, MA

Kristen L. Billiar

Worcester Polytechnic Institute, Worcester, MAUniversity of Massachusetts Medical School, Worcester, MA

Paper No. SBC2013-14100, pp. V01AT02A002; 2 pages
  • 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


Heart valve disease leads to approximately 300,000 heart valve replacement surgeries each year worldwide. Valvular interstitial cells (VICs) are believed to play a vital role in the repair of heart valves and also most disease processes. VICs synthesize, remodel, and repair the ECM; however, when VICs excessively differentiate to the highly contractile and synthetic myofibroblast phenotype, valvular fibrosis may ensue. Elevated mechanical stress triggers the differentiation of VICs into myofibroblasts. Transforming growth factor beta-1 (TGF-β1) is also critical for the formation of thicker stress fibers positive for α-smooth muscle actin (α-SMA), the defining characteristic of myofibroblasts.

Copyright © 2013 by ASME



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