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TENSEGRITY: THE ARCHITECTURAL BASIS OF CELLULAR MECHANOTRANSDUCTION

TENSEGRITY: THE ARCHITECTURAL BASIS OF CELLULAR MECHANOTRANSDUCTION ▪ Abstract Physical forces of gravity, hemodynamic stresses, and movement play a critical role in tissue development. Yet, little is known about how cells convert these mechanical signals into a chemical response. This review attempts to place the potential molecular mediators of mechanotransduction (e.g. stretch-sensitive ion channels, signaling mollecules, cytoskeleton, integrins) within the context of the structural complexity of living cells. The model presented relies on recent experimental findings, which suggests that cells use tensegrity architecture for their organization. Tensegrity predicts that cells are hard-wired to respond immediately to mechanical stresses transmitted over cell surface receptors that physically couple the cytoskeleton to extracellular matrix (e.g. integrins) or to other cells (cadherins, selectins, CAMs). Many signal transducing molecules that are activated by cell binding to growth factors and extracellular matrix associate with cytoskeletal scaffolds within focal adhesion complexes. Mechanical signals, therefore, may be integrated with other environmental signals and transduced into a biochemical response through force-dependent changes in scaffold geometry or molecular mechanics. Tensegrity also provides a mechanism to focus mechanical energy on molecular transducers and to orchestrate and tune the cellular response. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Annual Review of Physiology Annual Reviews

TENSEGRITY: THE ARCHITECTURAL BASIS OF CELLULAR MECHANOTRANSDUCTION

Ingber, D. E.
Annual Review of Physiology , Volume 59 (1) – Mar 1, 1997
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Publisher
Annual Reviews
Copyright
Copyright © 1997 by Annual Reviews Inc. All rights reserved
Subject
Review Articles
ISSN
0066-4278
eISSN
1545-1585
DOI
10.1146/annurev.physiol.59.1.575
pmid
9074778
Publisher site
See Article on Publisher Site

Abstract

▪ Abstract Physical forces of gravity, hemodynamic stresses, and movement play a critical role in tissue development. Yet, little is known about how cells convert these mechanical signals into a chemical response. This review attempts to place the potential molecular mediators of mechanotransduction (e.g. stretch-sensitive ion channels, signaling mollecules, cytoskeleton, integrins) within the context of the structural complexity of living cells. The model presented relies on recent experimental findings, which suggests that cells use tensegrity architecture for their organization. Tensegrity predicts that cells are hard-wired to respond immediately to mechanical stresses transmitted over cell surface receptors that physically couple the cytoskeleton to extracellular matrix (e.g. integrins) or to other cells (cadherins, selectins, CAMs). Many signal transducing molecules that are activated by cell binding to growth factors and extracellular matrix associate with cytoskeletal scaffolds within focal adhesion complexes. Mechanical signals, therefore, may be integrated with other environmental signals and transduced into a biochemical response through force-dependent changes in scaffold geometry or molecular mechanics. Tensegrity also provides a mechanism to focus mechanical energy on molecular transducers and to orchestrate and tune the cellular response.

Journal

Annual Review of Physiology – Annual Reviews

Published: Mar 1, 1997

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