Shear stress induced

A shear stress induces a shear strain. If a cube shears sideways by an amount w then the shear strain is defined by... 

Miyagi, M., et al. (2005). Activator protein-1 mediates shear stress-induced prostaglandin d synthase gene expression in vascular endothelial cells. Arterioscler. Thromb. Vase. Biol. 25, 970-5. 

Taba, Y., et al. (2000). Fluid shear stress induces lipocalin-type prostaglandin D2 synthase expression in vascular endothelial cells. Circul. Res. 86, 967-73. 

Moake, J. L., Turner, N. A., Stathopoulos, N. A., Nolasco, L., and Heliums, J. D., Involvement of large plasma von Willebrand factor (vWF) multimers and unusually large vWF forms derived from endothelial cells in shear-stress induced platelet aggregation. J. Clin. Invest. 78,1456-1461... 

Buga, G. M., Gold, M. E., Fukuto, J. M., and Ignarro, L. J. (1991). Shear-stress-induced release of nitric oxide from endothelial cells grown on beads. Hypertension (Dallas) 17, 187-193. 

Kamioka H, Sugawara Y, Murshid SA, Ishihara Y, Honjo T, Takano-Yamamoto T. 2006. Fluid shear stress induces less calcium response in a single primary osteocyte than in a single osteoblast implication of different focal adhesion formation. J Bone Miner Res 21 1012—21. 

Nomura S, Tandon NN, Nakamura T, Cone J, Fukuhara S, Kambayashi J. High-shear-stress-induced activation of platelets and microparticles enhances expression of cell adhesion molecules in THP-1 and endothelial cells. Atherosclerosis 2001 158 277-287. 

Mi. L.Y., Basu, M., Fritton, S.P., Cowin, S.C. (2004a) Analysis of avian bone response to mechanical loading Part One Distribution of bone fluid shear stress induced by bending and axial loading, in preparation. 

Brakemeier, S., Kersten, A., Eichler, I., Grgic, I., Zakrzewicz, A., Hopp, H., Kohler, R., and Hoyer, J. 2003. Shear stress-induced up-regulation of the intermediate-conductance Ca2+-activated K+ channel in human endothelium. Cardiovasc. Res. 60 488 196. 

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. 

Gloe T, Sohn HY, Meininger GA, Pohl U. Shear stress-induced release of basic fibroblast growth factor from endothelial cells is mediated by matrix interaction via integrin ocv 33. J Biol Chem. 2002 277 23453-23458. 

The authors [116] showed that the structure of high thermal stability, such as the ordered layered structure ofHT-LiCoOi, can be easily distorted with the help of the shearing stress induced by grinding, according to the following reaction ... 

In Figures lb and Ic relative motion exists between the droplet and the gas stream such that internal circulation is estabhshed through the shear stress induced at the nonrigid interface. Nonradial transports are important in the present cases, particularly for the momentum transport. Separation and reverse flow may (Figure Ic) or may not (Figure lb) occur, although the analysis is expected to be greatly complicated for the former case. 

K. Ayajiki, M. Kindermann, M. Hecker, 1. Fleming and R. Busse, Intracellular pH and tyrosine phosphorylation but not calcium determine shear-stress induced nitric oxide production in native endothelial cells. Circ Res 78, 750-758 (1996). 

M.-C. Aubert, M.-P. Elluard and H. Barnier, Shear stress induced erosion of filrtration cake studied by a flat rotating disk method. Determination of the critical shear stress of erosion. /. Membr. Sci., 84 (1993) 229. 

An analysis of the contributions to the skin friction shows that the surface waves play the dominant role. The shear stress induced by bottom currents exceeds the low fluff threshold only occasionally, especially during inflow events of saline water through the narrow channels. Therefore, an estimation of the resuspension potential of bottom sediments may be based on waves only, as, for instance, done by Jonsson (2006). However, without bottom currents some events will be missing, and, more important, no conclusions about the transport paths are possible. 

Occludin phosphorylation may provide a molecular mechanism to control barrier properties. Studies from our group have demonstrated that both VEGF and shear stress induce permeability across endothelial monolayers associated with a rapid phosphorylation of occludin (67,68). The occludin phosphorylation was attenuated by a non-hydrolyzable cAMP analog that also inhibits shear-induced permeability (68). This phosphorylation of occludin appears to be serine or threonine directed since immunoprecipitation of occludin and phosphotyrosine blotting did not reveal any evidence of occludin tyrosine phosphorylation in this cell system (unpublished observation). However, in epithelial cells, evidence of occludin tyrosine phosphorylation exists (69). In addition, others have identified occludin phosphorylation in response to histamine (70) and use of brain extracts has helped identify casein kinase II as an occludin kinase (71). Collectively, this work demonstrates a close association of occludin phosphorylation with permeability. Future studies identifying specific occludin phosphorylation sites, followed by mutational analysis, should reveal the functional significance of occludin phosphorylation. 

Morita, T., Kurihara, H., Maemura, K., Yoshizutni, M., and Yazaki, Y. (1993a). Disruption of cytoskeletal structures mediates shear stress-induced endothelin-1 gene expression in cultured porcine aortic endothelial cells.. Clin. Invest. 92, 1706-1712. 

Ranjan, V., and Diamond, S. L. (1993). Fluid shear stress induces synthesis and nuclear localization of c-fos in cultured human endothelial cells. Biochem. Biophys. Res. Commun. 196, 79-84. 

Schwarz, G., Droogmans, G., and Nilius, B. (1992). Shear stress induced membrane currents and calcium transients in human vascular endothelial cells. Pfluegers Arch. 421,394-396. 

Shyy, Y.-J., Hsieh, H.-J., Usami, S., and Chien, S. (1994). Fluid shear stress induces a biphasic response of human monocyte chemotactic protein 1 gene expression in vascular endothelium. Proc. Natl. Acad. Sci. U.S.A. 91, 4678-4682. 

FIGURE 2 Inhibition of shear stress-induced release of nitric oxide in isolated endothelial cells by S-nitroso-N-acetylpenicillamine (SNAP). Relaxant responses of the first arterial strip in a three-tissue cascade are illustrated. The flow rate through the column of endothelial cells was varied from 0.3 to 3 ml/min. Three sets of control responses were obtained at 15-min intervals before the addition of SNAP. After the third set of control responses, 1 /rmol/liter SNAP was perfused through the column for 15 min (positioned away from the target arterial strips), following which the column was perfused with plain Krebs bicarbonate solution for a further 15 min. The perfusate was then directed over the target strips, and responses to shear stress were obtained. Data represent the means se from at least four separate experiments. 

Shear stress induces larger amounts of elastin in cells and inhibits tissue calcification. Occludin, a transmembrane protein that forms tight junctions between cells, and is the main contributor to the blood-brain barrier (an obstacle to free passage of complex molecules into the central nervous system), is present in lesser amounts at high shear stress values (about 10% less at 20-30 dynes/cm ). 

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