Open Access

ARTICLE

Short-Term Shear Stress Induces Rapid Actin Dynamics in Living Endothelial Cells

Colin K. Choi^*, Brian P. Helmke^∗,†

∗ Department of Biomedical Engineering and Robert M.Berne Cardiovascular Research Center, University of Virginia, Charlottesville, Virginia, USA
† Corresponding author. Phone: +1 434-924-1726; Fax: +1 434-982-3870; Email: helmke@virginia.edu

Molecular & Cellular Biomechanics 2008, 5(4), 247-258. https://doi.org/10.3970/mcb.2008.005.247

Abstract

Hemodynamic shear stress guides a variety of endothelial phenotype characteristics, including cell morphology, cytoskeletal structure, and gene expression profile. The sensing and processing of extracellular fluid forces may be mediated by mechanotransmission through the actin cytoskeleton network to intracellular locations of signal initiation. In this study, we identify rapid actin-mediated morphological changes in living subconfluent and confluent bovine aortic endothelial cells (ECs) in response to onset of unidirectional steady fluid shear stress (15 dyn/cm²). After flow onset, subconfluent cells exhibited dynamic edge activity in lamellipodia and small ruffles in the downstream and side directions for the first 12 min; activity was minimal in the upstream direction. After 12 min, peripheral edge extension subsided. Confluent cell monolayers that were exposed to shear stress exhibited only subtle increases in edge fluctuations after flow onset. Addition of cytochalasin D to disrupt actin polymerization served to suppress the magnitude of flow-mediated actin remodeling in both subconfluent confluent EC monolayers. Interestingly, when subconfluent ECs were exposed to two sequential flow step increases (1 dyn/cm² followed by 15 dyn/cm² 12 min later), actin-mediated edge activity was not additionally increased after the second flow step. Thus, repeated flow increases served to desensitize mechanosensitive structural dynamics in the actin cytoskeleton.

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