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Flow‐induced mechanotransmission from the endothelial cytoskeleton to extracellular matrix
Author(s) -
Evans Rachel E.,
Mott Rosalind E.,
Helmke Brian P.
Publication year - 2010
Publication title -
the faseb journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.709
H-Index - 277
eISSN - 1530-6860
pISSN - 0892-6638
DOI - 10.1096/fasebj.24.1_supplement.600.3
Subject(s) - fibronectin , vinculin , rhoa , extracellular matrix , microbiology and biotechnology , chemistry , shear stress , focal adhesion , cytoskeleton , biophysics , materials science , cell , biology , biochemistry , signal transduction , composite material
Dynamic integrin ligation and transient Rho GTPase inactivation are required for endothelial cell adaptation to hemodynamic shear stress, but bidirectional mechanosignaling mechanisms between extracellular matrix (ECM) and the cytoskeleton remain unknown. In this study, GFP‐vinculin and rhodamine‐fibronectin displacement were tracked simultaneously during a step increase from 0 to 12 dyn/cm 2 unidirectional shear stress. In postconfluent monolayers, shear stress onset caused downstream‐directed displacement of focal adhesions and fibronectin fibrils. Transient inactivation of RhoA after shear stress onset was mediated by activation of p190RhoGAP‐A. In subconfluent layers, displacement patterns after shear stress onset in fully assembled ECM were similar to those in confluent monolayers, and cell motility was increased. On partially assembled fibronectin, structural dynamics were arrested after shear stress onset. Overexpression of dominant‐negative p190RhoGAP‐A eliminated flow‐dependent cessation of displacement. These data suggest that shear stress regulates RhoA‐dependent mechanotransmission to the ECM via p190RhoGAP‐A. Supported by NIH grant HL080956.