scholarly journals Calpain 2 is activated downstream of wall shear stress and sphingosine‐1‐phosphate to induce endothelial cell sprout formation in three dimensional collagen matrices

2009 ◽  
Vol 23 (S1) ◽  
Author(s):  
Hojin Kang ◽  
Hyeongil Kwak ◽  
Roland Kaunas ◽  
Kayla Bayless
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Collagen Matrices ◽  
Sphingosine 1 Phosphate ◽  
Calpain 2 ◽  
Wall Shear ◽  
Sprout Formation

scholarly journals Bicuspid Aortic Cusp Fusion Morphology Alters Aortic Three-Dimensional Outflow Patterns, Wall Shear Stress, and Expression of Aortopathy

Circulation ◽  
2014 ◽  
Vol 129 (6) ◽  
pp. 673-682 ◽  
Author(s):  
Riti Mahadevia ◽  
Alex J. Barker ◽  
Susanne Schnell ◽  
Pegah Entezari ◽  
Preeti Kansal ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Aortic Cusp ◽  
Wall Shear

scholarly journals Piezo1 mediates angiogenesis through activation of MT1-MMP signaling

2019 ◽  
Vol 316 (1) ◽  
pp. C92-C103 ◽  
Author(s):  
Hojin Kang ◽  
Zhigang Hong ◽  
Ming Zhong ◽  
Jennifer Klomp ◽  
Kayla J. Bayless ◽  
...  
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Matrix Metalloproteinase ◽  
Matrix Metalloproteinase 2 ◽  
Sprouting Angiogenesis ◽  
Sphingosine 1 Phosphate ◽  
Wall Shear ◽  
Membrane Type

Angiogenesis is initiated in response to a variety of external cues, including mechanical and biochemical stimuli; however, the underlying signaling mechanisms remain unclear. Here, we investigated the proangiogenic role of the endothelial mechanosensor Piezo1. Genetic deletion and pharmacological inhibition of Piezo1 reduced endothelial sprouting and lumen formation induced by wall shear stress and proangiogenic mediator sphingosine 1-phosphate, whereas Piezo1 activation by selective Piezo1 activator Yoda1 enhanced sprouting angiogenesis. Similarly to wall shear stress, sphingosine 1-phosphate functioned by activating the Ca2+ gating function of Piezo1, which in turn signaled the activation of the matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase during sprouting angiogenesis. Studies in mice in which Piezo1 was conditionally deleted in endothelial cells demonstrated the requisite role of sphingosine 1-phosphate-dependent activation of Piezo1 in mediating angiogenesis in vivo. These results taken together suggest that both mechanical and biochemical stimuli trigger Piezo1-mediated Ca2+ influx and thereby activate matrix metalloproteinase-2 and membrane type 1 matrix metalloproteinase and synergistically facilitate sprouting angiogenesis.

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.

Inflammatory Response of Endothelial Cells to Wall Shear Stress in Three Dimensional Stenotic Models

2009 ◽  
Author(s):  
Leonie Rouleau ◽  
Joanna Rossi ◽  
Jean-Claude Tardif ◽  
Rosaire Mongrain ◽  
Richard L. Leask
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Realistic Model ◽  
In Vitro Models ◽  
Steady Flows ◽  
Wall Shear

Endothelial cells (ECs) are believed to respond differentially to hemodynamic forces in the vascular tree. Once atherosclerotic plaque has formed in a vessel, the obstruction creates complex spatial gradients in wall shear stress (WSS). In vitro models have used mostly unrealistic and simplified geometries, which cannot reproduce accurately physiological conditions. The objective of this study was to expose ECs to the complex WSS pattern created by an asymmetric stenosis. Endothelial cells were grown and exposed for different times to physiological steady flows in straight dynamic controls and in idealized asymmetric stenosis models. Cell morphology was noticeably different in the regions with spatial WSS gradients, being more randomly oriented and of cobblestone shape. Inflammatory molecule expression was also altered by exposure to shear and endothelial nitric oxide synthase (eNOS) was upregulated by its presence. A regional response in terms of inflammation was observed through confocal microscopy. This work provides a more realistic model to study endothelial cell response to spatial and temporal WSS gradients that are present in vivo and is an important advancement towards a better understanding of the mechanisms involved in coronary artery disease.

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.

Three-dimensional vortical structures and wall shear stress in a curved artery model

2019 ◽  
Vol 31 (12) ◽  
pp. 121903 ◽  
Author(s):  
Christopher Cox ◽  
Mohammad Reza Najjari ◽  
Michael W. Plesniak
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Vortical Structures ◽  
Curved Artery ◽  
Wall Shear

scholarly journals Measurements of the wall shear stress distribution in the outflow tract of an embryonic chicken heart

2009 ◽  
Vol 7 (42) ◽  
pp. 91-103 ◽  
Author(s):  
C. Poelma ◽  
K. Van der Heiden ◽  
B. P. Hierck ◽  
R. E. Poelmann ◽  
J. Westerweel
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Three Dimensional ◽  
Outflow Tract ◽  
Chicken Heart ◽  
Embryonic Chicken ◽  
Dimensional Reconstruction ◽  
Wall Shear ◽  
Embryo Heart

In order to study the role of blood–tissue interaction in the developing chicken embryo heart, detailed information about the haemodynamic forces is needed. In this study, we present the first in vivo measurements of the three-dimensional distribution of wall shear stress (WSS) in the outflow tract (OFT) of an embryonic chicken heart. The data are obtained in a two-step process: first, the three-dimensional flow fields are measured during the cardiac cycle using scanning microscopic particle image velocimetry; second, the location of the wall and the WSS are determined by post-processing flow velocity data (finding velocity gradients at locations where the flow approaches zero). The results are a three-dimensional reconstruction of the geometry, with a spatial resolution of 15–20 µm, and provides detailed information about the WSS in the OFT. The most significant error is the location of the wall, which results in an estimate of the uncertainty in the WSS values of 20 per cent.

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