Temporal evolution of cell focal adhesions: experimental observations and shear stress profiles

Measurements with both two-dimensional (2D) two-component and three-component stereo particle image velocimetry (PIV) and computation in 2D and three-dimensional (3D) using Reynolds stress turbulence model with commercial code are carried out in a square duct backward-facing step (BFS) in a turbulent water flow at three Reynolds numbers of about 12,000, 21,000, and 55,000 based on the step height h and the inlet streamwise maximum mean velocity U0. The reattachment locations measured at a distance of Δy=0.0322h from the wall are 5.3h, 5.6h, and 5.7h, respectively. The inlet flow condition is fully developed duct flow before the step change with the expansion ratio of 1.2. PIV results show that the mean velocity, root mean square (rms) velocity profiles, and Reynolds shear stress profiles in all the experimental flow cases are almost identical in the separated shear-layer region when they are nondimensionalized by U0. The sidewall effect of the square BFS flow is analyzed by comparing the experimental statistics with direct numerical simulation (DNS) and Reynolds stress model (RSM) data. For this purpose, the simulation is carried out for both 2D BFS and for square BFS having the same geometry in the 3D case as the experimental case at the lowest Reynolds number. A clear difference is observed in rms and Reynolds shear stress profiles between square BFS experimental results and DNS results in 2D channel in the spanwise direction. The spanwise rms velocity difference is about 30%, with experimental tests showing higher values than DNS, while in contrast, turbulence intensities in streamwise and vertical directions show slightly lower values than DNS. However, with the modeling, the turbulence statistical differences between 2D and 3D RSM cases are very modest. The square BFS indicates 0.5h–1.5h smaller reattachment distances than the reattachment lengths of 2D flow cases.

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High Glucose Alters Endothelial Cell Response to Shear Stress

ASME 2009 Summer Bioengineering Conference, Parts A and B ◽

10.1115/sbc2009-206531 ◽

2009 ◽

Author(s):

Steven F. Kemeny ◽

Alisa Morss Clyne

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Endothelial Cell ◽

Blood Vessels ◽

Cell Mechanics ◽

High Glucose ◽

Fluid Shear Stress ◽

Cell Function ◽

Focal Adhesions ◽

Endothelial Cell Function

Endothelial cells line the walls of all blood vessels, where they maintain homeostasis through control of vascular tone, permeability, inflammation, and the growth and regression of blood vessels. Endothelial cells are mechanosensitive to fluid shear stress, elongating and aligning in the flow direction [1–2]. This shape change is driven by rearrangement of the actin cytoskeleton and focal adhesions [2]. Hyperglycemia, a hallmark of diabetes, affects endothelial cell function. High glucose has been shown to increase protein kinase C, formation of glucose-derived advanced glycation end-products, and glucose flux through the aldose reductase pathway within endothelial cells [3]. These changes are thought to be related to increased reactive oxygen species production [4]. While endothelial cell mechanics have been widely studied in healthy conditions, many disease states have yet to be explored. Biochemical alterations related to high glucose may alter endothelial cell mechanics.

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Molecular Control of Cytoskeletal Mechanics by Hemodynamic Forces

Physiology ◽

10.1152/physiol.00040.2004 ◽

2005 ◽

Vol 20 (1) ◽

pp. 43-53 ◽

Cited By ~ 41

Author(s):

Brian P. Helmke

Keyword(s):

Shear Stress ◽

Structural Dynamics ◽

Molecular Level ◽

Physiological Function ◽

Primary Transducer ◽

Molecular Control ◽

Hemodynamic Forces ◽

Spatial Gradients ◽

Cellular Mechanotransduction ◽

Stress Profiles

The endothelium at the interface between blood and tissue acts as a primary transducer of local hemodynamic forces into signals that maintain physiological function or initiate pathological processes in vessel walls. Rapid intracellular spatial gradients of structural dynamics and signaling molecule activity suggest that mechanical cues at the molecular level guide cellular mechanotransduction and adaptation to shear stress profiles.

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Evaluation of electro-osmotic flow in a nanochannel via semi-analytical method

Thermal Science ◽

10.2298/tsci1205297j ◽

2012 ◽

Vol 16 (5) ◽

pp. 1297-1302 ◽

Cited By ~ 6

Author(s):

Payam Jalili ◽

Domairry Ganji ◽

Bahram Jalili ◽

Domiri Ganji

Keyword(s):

Shear Stress ◽

Analytical Method ◽

Homotopy Perturbation Method ◽

Numerical Solutions ◽

Electrical Potential ◽

Osmotic Flow ◽

Homotopy Perturbation ◽

Stress Profiles ◽

Electro Osmotic Flow ◽

Cation Distributions

In this paper, equations due to anion and cation distributions, electrical potential and shear stress profiles in a nanochannel are formed for 1-D electro-osmotic flow, and solved by homotopy perturbation method. Results are compared with numerical solutions.

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A generalized form of the Saint-Venant equation with velocity and shear stress profiles

Journal of Hydraulic Research ◽

10.1080/00221689609498473 ◽

1996 ◽

Vol 34 (4) ◽

pp. 481-501

Author(s):

P. Hamm

Keyword(s):

Shear Stress ◽

Venant Equation ◽

Stress Profiles

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Eosinophil adhesion under flow conditions activates mechanosensitive signaling pathways in human endothelial cells

Journal of Experimental Medicine ◽

10.1084/jem.20041315 ◽

2005 ◽

Vol 202 (6) ◽

pp. 865-876 ◽

Cited By ~ 25

Author(s):

Susan L. Cuvelier ◽

Smitha Paul ◽

Neda Shariat ◽

Pina Colarusso ◽

Kamala D. Patel

Keyword(s):

Endothelial Cells ◽

Shear Stress ◽

Endothelial Cell ◽

Protein Kinase ◽

Leukocyte Adhesion ◽

Focal Adhesions ◽

Mitogen Activated Protein Kinase ◽

Flow Conditions ◽

Endothelial Cell Surface ◽

Mitogen Activated Protein

Leukocyte transmigration can be affected by shear stress; however, the mechanisms by which shear stress modulates transmigration are unknown. We found that adhesion of eosinophils or an eosinophilic cell line to intereukin 4–stimulated endothelial cells led to a shear-dependent increase in endothelial cell intracellular calcium and increased phosphorylation of extracellular signal-regulated kinase (ERK) 2, but not c-Jun NH2-terminal kinase or p38 mitogen-activated protein kinase. Latex beads coated with antibodies were used to characterize the role of specific endothelial cell surface molecules in initiating signaling under shear conditions. We found that ligation of either vascular cell adhesion molecule–1 or E-selectin, but not major histocompatibility complex class I, induced a shear-dependent increase in ERK2 phosphorylation in cytokine-stimulated endothelial cells. Disassembly of the actin cytoskeleton with latrunculin A prevented ERK2 phosphorylation after adhesion under flow conditions, supporting a role for the cytoskeleton in mechanosensing. Rapid phosphorylation of focal adhesion kinase and paxillin occurred under identical conditions, suggesting that focal adhesions were also involved in mechanotransduction. Finally, we found that Rho-associated protein kinase and calpain were both critical in the subsequent transendothelial migration of eosinophils under flow conditions. These data suggest that ligation of leukocyte adhesion molecules under flow conditions leads to mechanotransduction in endothelial cells, which can regulate subsequent leukocyte trafficking.

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The Effects of Fins on the Intermediate Wake of a Submarine Model

Journal of Fluids Engineering ◽

10.1115/1.4001010 ◽

2010 ◽

Vol 132 (3) ◽

Cited By ~ 13

Author(s):

Juan M. Jiménez ◽

Ryan T. Reynolds ◽

Alexander J. Smits

Keyword(s):

Shear Stress ◽

Velocity Profile ◽

Outer Region ◽

Reynolds Numbers ◽

Velocity Profiles ◽

Turbulent Wake ◽

Self Similar ◽

Stress Profiles

Results are presented on the behavior of the turbulent wake behind a submarine model for a range of Reynolds numbers based on the model length between 0.49×106 and 1.8×106, for test locations between 3 and 9 diameters downstream of the stern. The shape of the model emulates an idealized submarine, and tests were performed with and without stern fins. In the absence of fins, the velocity profile in planes away from the influence of the sail rapidly becomes self-similar and is well described by a function of exponentials. The fins create defects in the velocity profiles in the outer region of the wake, while yielding higher values of turbulence at locations corresponding to the tips of the fins. Measurements conducted in planes away from the midline plane show that the velocity profiles remain self-similar, while the shear stress profiles clearly show the effects of the necklace vortices trailing from the base of the fins.

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Podocytes are sensitive to fluid shear stress in vitro

AJP Renal Physiology ◽

10.1152/ajprenal.00196.2005 ◽

2006 ◽

Vol 291 (4) ◽

pp. F856-F865 ◽

Cited By ~ 76

Author(s):

Colin Friedrich ◽

Nicole Endlich ◽

Wilhelm Kriz ◽

Karlhans Endlich

Keyword(s):

Shear Stress ◽

Tyrosine Kinases ◽

Fluid Shear Stress ◽

Focal Adhesions ◽

Fluid Shear ◽

Cell Contacts ◽

Tk Inhibitors ◽

Static Conditions ◽

Cell Cell

Podocytes are exposed to mechanical forces arising from glomerular capillary pressure and filtration. It has been shown that stretch affects podocyte biology in vitro and plays a significant role in the development of glomerulosclerosis in vivo. However, whether podocytes are sensitive to fluid shear stress is completely unknown. In the present study, we therefore exposed cells of a recently generated conditionally immortalized mouse podocyte cell line to defined fluid shear stress in a flow chamber, mimicking flow of the glomerular ultrafiltrate over the surface of podocytes in Bowman's space. Shear stress above 0.25 dyne/cm2 resulted in dramatic loss of podocytes but not of proximal tubular epithelial cells (LLC-PK1 cells) after 20 h. At 0.015–0.25 dyne/cm2, lamellipodia formation in podocytes was enhanced and the actin nucleation protein cortactin was redistributed to the cell margins. Shear stress further diminished stress fibers and the presence of vinculin in focal adhesions. Linear zonula occludens-1 distribution at cell-cell contacts remained unaffected at low shear stress. At 0.25 dyne/cm2, the monolayer was broken up and remaining cell-cell contacts were reinforced by F-actin and α-actinin. Because the cytoskeletal changes induced by shear stress suggested the involvement of tyrosine kinases (TKs), we tested several TK inhibitors that were all without effect on podocyte number under static conditions. At 0.25 dyne/cm2, however, the TK inhibitors genistein and AG 82 were associated with marked podocyte loss. Our data demonstrate that podocytes are highly sensitive to fluid shear stress. Shear stress induces a reorganization of the actin cytoskeleton and activates specific tyrosine kinases that are required to withstand fluid shear stress.

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