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The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue

Mechanotransduction via the extracellular matrix (ECM)–myosin pathway is involved in determining cell morphology during development and in coupling external transient mechanical stimuli to the reorganization of the cytoskeleton. Here, we present a review on the molecular mechanisms involved in this...

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Detalles Bibliográficos
Autores principales: Popa, Ionel, Gutzman, Jennifer H.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Portland Press Ltd. 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289002/
https://www.ncbi.nlm.nih.gov/pubmed/33530663
http://dx.doi.org/10.1042/ETLS20180043
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author Popa, Ionel
Gutzman, Jennifer H.
author_facet Popa, Ionel
Gutzman, Jennifer H.
author_sort Popa, Ionel
collection PubMed
description Mechanotransduction via the extracellular matrix (ECM)–myosin pathway is involved in determining cell morphology during development and in coupling external transient mechanical stimuli to the reorganization of the cytoskeleton. Here, we present a review on the molecular mechanisms involved in this pathway and how they influence cellular development and organization. We investigate key proteins involved in the ECM–myosin pathway and discuss how specific binding events and conformational changes under force are related to mechanical signaling. We connect these molecular mechanisms with observed morphological changes at the cellular and organism level. Finally, we propose a model encompassing the biomechanical signals along the ECM–myosin pathway and how it could be involved in cell adhesion, cell migration, and tissue architecture.
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spelling pubmed-72890022020-06-18 The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue Popa, Ionel Gutzman, Jennifer H. Emerg Top Life Sci Review Articles Mechanotransduction via the extracellular matrix (ECM)–myosin pathway is involved in determining cell morphology during development and in coupling external transient mechanical stimuli to the reorganization of the cytoskeleton. Here, we present a review on the molecular mechanisms involved in this pathway and how they influence cellular development and organization. We investigate key proteins involved in the ECM–myosin pathway and discuss how specific binding events and conformational changes under force are related to mechanical signaling. We connect these molecular mechanisms with observed morphological changes at the cellular and organism level. Finally, we propose a model encompassing the biomechanical signals along the ECM–myosin pathway and how it could be involved in cell adhesion, cell migration, and tissue architecture. Portland Press Ltd. 2018-12-21 2018-12-21 /pmc/articles/PMC7289002/ /pubmed/33530663 http://dx.doi.org/10.1042/ETLS20180043 Text en © 2018 The Author(s) https://creativecommons.org/licenses/by-nc-nd/4.0/ This is an open access article published by Portland Press Limited on behalf of the Biochemical Society and the Royal Society of Biology and distributed under the Creative Commons Attribution License 4.0 (CC BY-NC-ND) (https://creativecommons.org/licenses/by-nc-nd/4.0/) .
spellingShingle Review Articles
Popa, Ionel
Gutzman, Jennifer H.
The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title_full The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title_fullStr The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title_full_unstemmed The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title_short The extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
title_sort extracellular matrix–myosin pathway in mechanotransduction: from molecule to tissue
topic Review Articles
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7289002/
https://www.ncbi.nlm.nih.gov/pubmed/33530663
http://dx.doi.org/10.1042/ETLS20180043
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