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Aging Endothelial Cells Exhibit Decreased Response to Atheroprotective Shear Stress

[+] Author Affiliations
Tracy M. Cheung, George A. Truskey

Duke University, Durham, NC

Paper No. SBC2013-14402, pp. V01AT04A011; 2 pages
doi:10.1115/SBC2013-14402
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

As endothelial cells (ECs) age, morphological and physiological changes occur that may alter macromolecular transport and cause subsequent disease development. ECs in atherosclerotic regions exhibit high cell turnover and high levels of oxidative stress due to transient flow patterns and low and oscillating shear stress. This leads to replicative or stress-induced senescence. Resveratrol indirectly reverses senescence-associated phenotypes via competitive inhibition of cAMP-degrading phosphodiesterases (PDEs). Elevated levels of membrane-associated cAMP activate the cyclic AMP-regulated guanosine nucleotide exchange factor Epac1 which, in turn, leads to guanosine triphosphate (GTP) binding to the small G protein Rap1. GTP bound Rap1 activates the deacetylase SIRTUIN1 (SIRT1) but also causes changes to the cortical cytoskeleton and organization of VE-cadherin mechanosensor in the endothelial junctions (Figure 1).

Copyright © 2013 by ASME

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