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Thu Dec 4

• BMC Immunology

Thu Oct 30

• ,ECHANISM FOR HETEROGEN endohelial RESPONSES TO FL0: Exposure of endothelium to a nominally uniform flow field in viva and in vitro frequently results in a heterogeneous distribution of individual cell responses. Extremes in response levels are often noted in neighboring cells. Such variations are important for the spatial interpretation of vascular responses to flow and for an understanding of mechanotransdu ction mechanisms at the level of single cells. We propose that variations of local forces defined by the cell surface geometry contribute to these differences. Atomic force microscopy measurements of cell surface topography in living endothelium both in vitro and in situ combined with computational fluid dynamics demonstrated large cell-to-cell variations in the distribution of flow-generated shear stresses at the endothelial luminal surface. The distribution of forces throughout the surface of individual cells of the monolayer was also found to vary considerably and
• Flow-mediated endothelial mechanotransdu ction: Mechanical forces associated with blood flow play important roles in the acute control of vascular tone, the regulation of arterial structure and remodeling, and the localization of atheroscleroti c lesions. Major regulation of the blood vessel responses occurs by the action of hemodynamic shear stresses on the endothelium. The transmission of hemodynamic forces throughout the endothelium and the mechanotransdu ction mechanisms that lead to biophysical, biochemical, and gene regulatory responses of endothelial cells to hemodynamic shear stresses are reviewed.
• Subcellular distribution of shear stress at the surface of flow-aligned and nonaligned endothelial monolayers

Wed Oct 29

• Multiple Signaling Pathways in Flow-Mediated Endothelial Mechanotransdu ction: The endothelial monolayer is a signal transduction interface for blood-borne mechanical as well as chemical stimuli. The structural deformation arising from a mechanical stimulus, such as a change of hemodynamic shear stress, is conceptually different from the binding of a hormone or other agonist to its specific receptor, yet both elicit important endothelial signaling responses. Mechanical and chemical signaling appear to use common as well as unique pathways downstream of the initial stimulus. For example, signaling pathways arising from membrane deformation and hormone-recept or coupling may appear to converge through activation of phospholipases 1 or nuclear factor {kappa}B transcription factor complex2 but later diverge at the level of DNA binding3 (Figure 1). However, simple interpretation s of mechanotransdu ction are confounded by intracellular and pericellular force transfer, principally by the cytoskeleton,4 ,5 that results in the generation of transduction pathways at multiple
• The convergence of haemodynamics, genomics, and endothelial structure in studies of the focal origin of atherosclerosi s: The completion of the Human Genome Project and ongoing sequencing of mouse, rat and other genomes has led to an explosion of genetics-relat ed technologies that are finding their way into all areas of biological research; the field of biorheology is no exception. Here we outline how two disparate modern molecular techniques, microarray analyses of gene expression and real-time spatial imaging of living cell structures, are being utilized in studies of endothelial mechanotransdu ction associated with controlled shear stress in vitro and haemodynamics in vivo. We emphasize the value of such techniques as components of an integrated understanding of vascular rheology. In mechanotransdu ction, a systems approach is recommended that encompasses fluid dynamics, cell biomechanics, live cell imaging, and the biochemical, cell biology and molecular biology methods that now encompass genomics. Microarrays are a useful and powerful tool for such integration by identifying simultaneous changes in the
• Dual effect of fluid shear stress on volume-regulat ed anion current in bovine aortic endothelial cells: The key mechanism responsible for maintaining cell volume homeostasis is activation of volume-regulat ed anion current (VRAC). The role of hemodynamic shear stress in the regulation of VRAC in bovine aortic endothelial cells was investigated. We showed that acute changes in shear stress have a biphasic effect on the development of VRAC. A shear stress step from a background flow (0.1 dyn/cm2) to 1 dyn/cm2 enhanced VRAC activation induced by an osmotic challenge. Flow alone, in the absence of osmotic stress, did not induce VRAC activation. Increasing the shear stress to 3 dyn/cm2, however, resulted in only a transient increase of VRAC activity followed by an inhibitory phase during which VRAC was gradually suppressed. When shear stress was increased further (5-10 dyn/cm2), Our findings suggest that shear stress is an important factor in regulating the ability of vascular endothelial cells to maintain volume homeostasis.
• The Cytoskeleton Under External Fluid Mechanical Forces:: The endothelium, a single layer of cells that lines all blood vessels, is the focus of intense interest in biomechanics because it is the principal recipient of hemodynamic shear stress. In arteries, shear stress has been demonstrated to regulate both acute vasoregulation and chronic adaptive vessel remodeling and is strongly implicated in the localization of atheroscleroti c lesions. Thus, endothelial biomechanics and the associated mechanotransdu ction of shear stress are of great importance in vascular physiology and pathology. Here we discuss the important role of the cytoskeleton in a decentralizati on model of endothelial mechanotransdu ction. In particular, recent studies of four-dimension al cytoskeletal motion in living cells under external fluid mechanical forces are summarized together with new data on the spatial distribution of cytoskeletal strain. These quantitative studies strongly support the decentralized distribution of luminally imposed forces throughout the EC.
• Mapping Mechanical Strain of an Endogenous Cytoskeletal: A central aspect of cellular mechanochemica l signaling is a change of cytoskeletal tension upon the imposition of exogenous forces. Here we report measurements of the spatiotemporal distribution of mechanical strain in the intermediate filament cytoskeleton of endothelial cells computed from the relative displacement of endogenous green fluorescent protein (GFP)-vimentin before and after onset of shear stress. Quantitative image analysis permitted computation of the principal values and orientations of Lagrangian strain from 3-D high-resolutio n fluorescence intensity distributions that described intermediate filament positions. Spatially localized peaks in intermediate filament strain were repositioned after onset of shear stress. The orientation of principal strain indicated that mechanical stretching was induced across cell boundaries. This novel approach for intracellular strain mapping using an endogenous reporter demonstrates force transfer from lumenal surface throughout cell.
• Aortic Valve: Turning Over a New Leaf(let) in Endothelial Phenotypic ...: Editorial

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