S1P Synergizes with Wall Shear Stress and Other Angiogenic Factors to Induce Endothelial Cell Sprouting Responses

2017 ◽  
pp. 99-115 ◽  
Author(s):  
Camille L. Duran ◽  
Roland Kaunas ◽  
Kayla J. Bayless
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Angiogenic Factors ◽  
Wall Shear

Study on Velocity Distribution Estimation Using Blood Pressure Data Based on the Coupled Wave Theory of Elastic Pipes and Fluids

2019 ◽  
Author(s):  
Takeshi Tokunaga ◽  
Koji Mori ◽  
Hiroko Kadowaki ◽  
Takashi Saito
Keyword(s):  
Blood Pressure ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Cell Function ◽  
Wave Theory ◽  
Pressure Data ◽  
Endothelial Cell Function ◽  
Blood Pressure Data ◽  
Wall Shear

Abstract Cardiovascular disease that is one of Non-Communicable Disease accounts for about 25% of death in Japan. Prevention of arteriosclerosis that is a main cause of cardiovascular disease is important. Since an early lesions of arteriosclerosis progress as functional change of an endothelial cell that is uniformly distributed on the luminal surface of a blood vessel, an accurate evaluation of the endothelial cell function is important as prevention of the arteriosclerosis. Although Flow-Mediated Dilation (FMD) is widely used as a diagnosis of the endothelial cell function in clinic, it is an evaluation method that uses a static diameter of a blood vessel. Moreover, it isn’t possible to take into account individual difference of a wall shear stress on the endothelial cell. In previous study, it is found that an evoked hyperemic wall shear stress is a major correlate of %FMD. In order to accurately measure the endothelial cell function, it is necessary to simply assess the hyperemic shear stress during FMD. However, it is difficult to non-invasively measure the hyperemic shear stress on the endothelial cell in clinic. In this study, we focused on a blood pressure data that is obtained non-invasively and formulated a relationship between the pressure and a flow velocity based on the coupled wave theory. And we estimated a hyperemic shear stress by using a blood pressure data that is obtained by a tonometry method in experiment that simulate FMD. As a result of estimating the hyperemic shear stress, it reflected characteristics of blood flow in clinic. It may be necessary to consider the hyperemic pressure fluctuation that is waves including low frequency components. Moreover, the hyperemic pressure fluctuation should not be treated as a waveform that has individually different a static pressure in estimation of the hyperemic wall shear stress.

Effects of Steady Spatial Wall Shear Stress Gradients on Endothelial Cell Morphology in Three-Dimensional Models

2007 ◽  
Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Cell Morphology ◽  
Flow Direction ◽  
Stress Gradient ◽  
Spatial Gradient ◽  
Stress Gradients ◽  
Wall Shear

Endothelial cell (EC) dysfunction has been linked to atherosclerosis through their response to hemodynamic forces. Flow in stenotic vessels creates complex spatial gradients in wall shear stress. In vitro studies examining the effect of shear stress on endothelial cells have used unrealistic and simplified models, which cannot reproduce physiological conditions. The objective of this study was to expose endothelial cells to the complex shear shear pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flow in straight dynamic controls and in idealized asymmetric stenosis models. Cells subjected to 1D flow aligned with flow direction and had a spindle-like shape when compared to static controls. Endothelial cell morphology was noticeable different in the regions with a spatial gradient in wall shear stress, being more randomly oriented and of cobblestone shape. This occurred despite the presence of an increased magnitude in shear stress. No other study to date has described this morphology in the presence of a positive wall shear stress gradient or gradient of significant shear magnitude. This technique provides a more realistic model to study endothelial cell response to spatial and temporal shear stress gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.

Endothelial Cell Morphologic Response to Asymmetric Stenosis Hemodynamics: Effects of Spatial Wall Shear Stress Gradients

2010 ◽  
Vol 132 (8) ◽  
Author(s):  
Leonie Rouleau ◽  
Monica Farcas ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Atherosclerotic Plaque ◽  
Morphological Changes ◽  
Stress Gradients ◽  
Spatial Gradients ◽  
Wall Shear

Endothelial cells are known to respond to hemodynamic forces. Their phenotype has been suggested to differ between atheroprone and atheroprotective regions of the vasculature, which are characterized by the local hemodynamic environment. Once an atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress. Endothelial cell response to wall shear stress may be linked to the stability of coronary plaques. Unfortunately, in vitro studies of the endothelial cell involvement in plaque stability have been limited by unrealistic and simplified geometries, which cannot reproduce accurately the hemodynamics created by a coronary stenosis. Hence, in an attempt to better replicate the spatial wall shear stress gradient patterns in an atherosclerotic region, a three dimensional asymmetric stenosis model was created. Human abdominal aortic endothelial cells were exposed to steady flow (Re=50, 100, and 200 and τ=4.5 dyn/cm2, 9 dyn/cm2, and 18 dyn/cm2) in idealized 50% asymmetric stenosis and straight/tubular in vitro models. Local morphological changes that occur due to magnitude, duration, and spatial gradients were quantified to identify differences in cell response. In the one dimensional flow regions, where flow is fully developed and uniform wall shear stress is observed, cells aligned in flow direction and had a spindlelike shape when compared with static controls. Morphological changes were progressive and a function of time and magnitude in these regions. Cells were more randomly oriented and had a more cobblestone shape in regions of spatial wall shear stress gradients. These regions were present, both proximal and distal, at the stenosis and on the wall opposite to the stenosis. The response of endothelial cells to spatial wall shear stress gradients both in regions of acceleration and deceleration and without flow recirculation has not been previously reported. This study shows the dependence of endothelial cell morphology on spatial wall shear stress gradients and demonstrates that care must be taken to account for altered phenotype due to geometric features. These results may help explain plaque stability, as cells in shoulder regions near an atherosclerotic plaque had a cobblestone morphology indicating that they may be more permeable to subendothelial transport and express prothrombotic factors, which would increase the risk of atherothrombosis.

scholarly journals Endothelial cell dilatory pathways link flow and wall shear stress in an intact arteriolar network

1996 ◽  
Vol 81 (5) ◽  
pp. 2105-2114 ◽  
Author(s):  
Mary D. S. Frame ◽  
Ingrid H. Sarelius
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Control Cell ◽  
Flow Distribution ◽  
Red Cell ◽  
Network Cell ◽  
Bifurcation Angle ◽  
Spatial Changes ◽  
Wall Shear

Frame, Mary D. S., and Ingrid H. Sarelius. Endothelial cell dilatory pathways link flow and wall shear stress in an intact arteriolar network. J. Appl. Physiol.81(5): 2105–2114, 1996.—Our purpose was to determine whether the endothelial cell-dependent dilatory pathways contribute to the regulation of flow distribution in an intact arteriolar network. Cell flow, wall shear stress (Tω), diameter, and bifurcation angle were determined for four sequential branches of a transverse arteriole in the superfused cremaster muscle of pentobaribtal sodium (Nembutal, 70 mg/kg)-anesthetized hamsters ( n = 51). Control cell flow was significantly greater into upstream than into downstream branches [1,561 ± 315 vs. 971 ± 200 (SE) cells/s, n = 12]. Tissue exposure to 50 μM N ω-nitro-l-arginine + 50 μM indomethacin (l-NNA + Indo) produced arteriolar constriction of 14 ± 4% and decreased flow into the transverse arteriole. More of the available cell flow was diverted to downstream branches, yet flow distribution remained unequal. Control Tω was higher upstream than downstream (31.3 ± 6.8 vs. 9.8 ± 1.5 dyn/cm2).l-NNA + Indo decreased Tω upstream and increased Tω downstream to become equal in all branches, in contrast to flow. To determine whether constriction in general induced the same changes, 5% O2 (8 ± 4% constriction) or 10−9 M norepinephrine (NE; 4 ± 3% constriction) was added to the tissue ( n = 7). With O2, flow was redistributed to become equal into each branch. With NE, flow decreased progressively more into the first three branches. The changes in flow distribution were thus predictable and dependent on the agonist. With O2 or NE, the spatial changes in flow were mirrored by spatial changes in Tω. Changes in diameter and in cell flux were not related forl-NNA + Indo ( r = 0.45), O2( r = 0.07), or NE ( r = 0.36). For all agonists, when the bifurcation angle increased, cell flow to the branch decreased significantly, whereas if the angle decreased, flow was relatively preserved; thus active changes in bifurcation angle may influence red cell distribution at arteriolar bifurcations. Thus, when the endothelial cell dilatory pathways were blocked, the changes in flow and in Tω were uncoupled; yet when they were intact, flow and Tω changed together.

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