Influence of Mechanical Forces on Vessel Wall Cells

3 Influence of Mechanical Forces on Vessel Wall Cells 

The manner by which shear stress-induced cellular changes occur in endothelial cells involves cell membrane and cytoskeletal molecules that lead to a shape change. The cytoskeleton contains actin filaments, intermediate filaments, and microtubules, all of which are restructured upon exposure to external force. Under stress conditions, actin filaments coalesce to form stress fibers that anchor at the focal contacts, which are adhesion sites at the cell substrate interface. 

Flow-dependent changes in vessel diameter contribute to the optimization of circulatory function and are mediated via shear stress-induced release of NO, vasodilator prostanoids, and a putative endothelium-derived hyperpolarization factor or EDHF (Griffith, 2002). There is growing evidence that NO/prostanoid-independent relaxations involve direct hetero-cellular signaling between endothelium and smooth muscle cells via gap junctions. 

4 Mechanochemical Transduction by Vascular Smooth Muscle Cells (VSMCs) 

Recently, it has been demonstrated that mechanical stress rapidly induced phosphorylation of PDGF receptor, activation of integrin receptor, stretch-activation of cation channels, and production of G proteins. Once mechanical stress was sensed, protein kinase C and MAPKs were activated, leading to increased c-fos and c-Jun gene expression and enhanced transcription factor AP-1 DNA binding activity. The application of physical forces also rapidly resulted in expression of MAPK phosphatase-1 (MKP-1), which inactivates MAPKs. 

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