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Role of the cytoskeleton in flow (shear stress)-induced dilation and remodeling in resistance arteries

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Abstract

Cytoskeletal proteins determine cell shape and integrity and membrane-bound structures connected to extracellular components allow tissue integrity. These structural elements have an active role in the interaction of blood vessels with their environment. Shear stress due to blood flow is the most important force stimulating the endothelium. The role of cytoskeletal proteins in endothelial responses to flow has been studied in resistance arteries using pharmacological tools and transgenic models. Shear stress activates extracellular “flow sensing” elements associated with a thick glycocalyx communicating the signal to membrane-bound complexes (integrins and/or dystrophin-dystroglycans) and to eNOS through a pathway involving the intermediate filament vimentin, the microtubule network and actin. When blood flow increases chronically the endothelium triggers diameter enlargement and medial hypertrophy. This is facilitated by the genetic absence of the intermediate filaments, vimentin and desmin suggesting that these elements oppose the process.

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Abbreviations

INSERM:

National Institute for Health and Medical Research

CNRS:

National Center for Scientific Research

FMD:

Flow-mediated dilation

NO:

Nitric oxide

ROS:

Reactive oxygen species

ONOO−:

Peroxynitrites

eNOS:

Endothelial NO-synthase

FMD:

Flow-mediated dilation

CAV1:

Caveolin-1

MMPs:

Metalloproteases

FAK:

Focal adhesion kinase

HSPs:

Heat shock proteins

ECM:

Extracellular matrix

AT1/2R:

Angiotensin II type 1 or 2 receptor

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Authors and Affiliations

  1. Department of Integrated Neurovascular Biology, INSERM, CNRS, CHU d’Angers and Université d’Angers, Angers, France

    Laurent Loufrani & Daniel Henrion

  2. Faculté de Médecine, UMR CNRS 6214, INSERM 771, Rue Haute de Reculée, 49045, Angers, France

    Daniel Henrion

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Loufrani, L., Henrion, D. Role of the cytoskeleton in flow (shear stress)-induced dilation and remodeling in resistance arteries. Med Biol Eng Comput 46, 451–460 (2008). https://doi.org/10.1007/s11517-008-0306-2

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