Résumés
Résumé
Les vaisseaux sanguins sont en permanence soumis à des contraintes mécaniques associées à la pression artérielle, de caractère pulsé, et au flux sanguin. Toute variation de ces contraintes est perçue au niveau des cellules vasculaires et se traduit par des modifications fonctionnelles et structurales des vaisseaux. De nombreux récepteurs, présents à la surface des cellules endothéliales, sont sensibles aux forces de cisaillement. Les intégrines, reliant la matrice extracellulaire aux sites d’adhérence focale et au cytosquelette, peuvent transmettre et moduler la tension mécanique dans la cellule. Par ailleurs, les contraintes mécaniques agissent sur les canaux ioniques, stimulent des récepteurs membranaires et induisent des cascades complexes d’événements biochimiques. De nombreuses voies intracellulaires, telles que la voie des MAP-kinases, sont activées par le flux sanguin et aboutissent à l’induction de facteurs de transcription qui contrôlent l’expression des gènes. Ainsi, par des mécanismes purement locaux, le vaisseau sanguin est capable de s’adapter à son environnement mécanique.
Summary
Blood vessels are permanently subjected to mechanical forces in the form of stretch and shear stress. Any alterations in the hemodynamic environment invariably produce transformations in the vessel wall that will aim to accommodate the new conditions and to ultimately restore basal levels of mechanical forces. Many receptors, present on the surface of endothelial cells, allow vessels to detect subtle changes in shear stress. Inside the cells, cytoskeletal proteins transmit and modulate the tension between integrins, focal adhesion sites, and the extracellular matrix. Besides inducing structural modifications, mechanical forces lead to changes in the ionic composition of cells, mediated by ion channels, stimulate various membrane receptors, and induce complex biochemical cascades. Many intracellular pathways such as the MAP kinase cascade are activated by shear stress and initiate via sequential phosphorylations the activation of transcription factors and subsequent gene expression. Thus, by purely local mechanisms, blood vessels are capable of true autonomic regulation which enables them to adapt to their mechanical environment.
Parties annexes
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