3-D Stress Analysis in Cultured Endothelial Cells Exposed to Fluid Shear Stress

1999 ◽  
Author(s):  
T. Ohashi ◽  
H. Sugawara ◽  
Y. Ishii ◽  
M. Sato
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Surface ◽  
Fluid Shear Stress ◽  
Flow Direction ◽  
Stress Distributions ◽  
Fluid Shear ◽  
Surface Geometry ◽  
Cultured Endothelial Cells

Abstract Under fluid shear stress, applied both in vivo and in vitro, vascular endothelial cells show morphological changes. After applying shear stress, cultured endothelial cells showed elongation and orientation to the flow direction (Kataoka et al., 1998). Moreover, statistical image analysis showed that intercellular F-actin distributions were confirmed to change depending on the shear stress and the flow direction. Thus, the endothelial cell morphology relates closely with the cytoskeletal structures. Intercellular stress distributions in the cells may be also accompanied by the reorganization of cytoskeletal structures. The use of both atomic force microscopy measurements (AFM) of endothelial cell surface topography and computational fluid dynamics of shear stress distributions acting on the cell surface, it has revealed that the surface geometry defined the detailed distribution of shear stress (Davies et al., 1995).

Effects of Fluid Shear Stress on Endothelial Cell Invasion Into Three-Dimensional Matrices

2007 ◽  
Author(s):  
Hojin Kang ◽  
Kayla J. Bayless ◽  
Roland Kaunas
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Cell Invasion ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cells ◽  
Umbilical Vein ◽  
Shear Stresses ◽  
Collagen Gels ◽  
Fluid Shear

We have previously developed a cell culture model to study the effects of angiogenic factors, such as sphingosine-1-phosphate (S1P), on the invasion of endothelial cells into the underlying extracellular matrix. In addition to biochemical stimuli, vascular endothelial cells are subjected to fluid shear stress due to blood flow. The present study is aimed at determining the effects of fluid shear stress on endothelial cell invasion into collagen gels. A device was constructed to apply well-defined fluid shear stresses to confluent human umbilical vein endothelial cells (HUVECs) seeded on collagen gels. Fluid shear stress induced significant increases in cell invasion with a maximal induction at ∼5 dyn/cm2. These results provide evidence that fluid shear stress is a significant stimulus for endothelial cell invasion and may play a role in regulating angiogenesis.

scholarly journals The effect of fluid shear stress on microfilaments of cultured endothelial cells.

1992 ◽  
Vol 34 (4) ◽  
pp. 445-453
Author(s):  
Norio Aita ◽  
Akira Fujimura ◽  
Hitoshi Yokosuka ◽  
Fumio Tsuzuku ◽  
Yohichiro Nozaka
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Cultured Endothelial Cells

scholarly journals MAGI1 Mediates eNOS Activation and NO Production in Endothelial Cells in Response to Fluid Shear Stress

Cells ◽  
2019 ◽  
Vol 8 (5) ◽  
pp. 388 ◽  
Author(s):  
Kedar Ghimire ◽  
Jelena Zaric ◽  
Begoña Alday-Parejo ◽  
Jochen Seebach ◽  
Mélanie Bousquenaud ◽  
...  
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Protein Kinase ◽  
Fluid Shear Stress ◽  
Adaptor Protein ◽  
No Production ◽  
Fluid Shear ◽  
Enos Phosphorylation

Fluid shear stress stimulates endothelial nitric oxide synthase (eNOS) activation and nitric oxide (NO) production through multiple kinases, including protein kinase A (PKA), AMP-activated protein kinase (AMPK), AKT and Ca2+/calmodulin-dependent protein kinase II (CaMKII). Membrane-associated guanylate kinase (MAGUK) with inverted domain structure-1 (MAGI1) is an adaptor protein that stabilizes epithelial and endothelial cell-cell contacts. The aim of this study was to assess the unknown role of endothelial cell MAGI1 in response to fluid shear stress. We show constitutive expression and co-localization of MAGI1 with vascular endothelial cadherin (VE-cadherin) in endothelial cells at cellular junctions under static and laminar flow conditions. Fluid shear stress increases MAGI1 expression. MAGI1 silencing perturbed flow-dependent responses, specifically, Krüppel-like factor 4 (KLF4) expression, endothelial cell alignment, eNOS phosphorylation and NO production. MAGI1 overexpression had opposite effects and induced phosphorylation of PKA, AMPK, and CAMKII. Pharmacological inhibition of PKA and AMPK prevented MAGI1-mediated eNOS phosphorylation. Consistently, MAGI1 silencing and PKA inhibition suppressed the flow-induced NO production. Endothelial cell-specific transgenic expression of MAGI1 induced PKA and eNOS phosphorylation in vivo and increased NO production ex vivo in isolated endothelial cells. In conclusion, we have identified endothelial cell MAGI1 as a previously unrecognized mediator of fluid shear stress-induced and PKA/AMPK dependent eNOS activation and NO production.

scholarly journals Piezo1 acts upstream of TRPV4 to induce pathological changes in endothelial cells due to shear stress

2020 ◽  
pp. jbc.RA120.015059
Author(s):  
Sandip M Swain ◽  
Rodger A Liddle
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Venous Pressure ◽  
Calcium Signal ◽  
Cell Integrity ◽  
Fluid Shear ◽  
Channel Opening ◽  
Trpv4 Channel

The ion channels Piezo1 and TRPV4 have both, independently, been implicated in high venous pressure- and fluid shear stress-induced vascular hyperpermeability in endothelial cells.  However, the mechanism by which Piezo1 and TRPV4 channels execute the same function is poorly understood.  Here we demonstrate that Piezo1 regulates TRPV4 channel activation in endothelial cells and that Piezo1-mediated TRPV4 channel opening is a function of the strength and duration of fluid shear stress.  We first confirmed that either fluid shear stress or the Piezo1 agonist, Yoda1, led to an elevation in intracellular calcium ([Ca2+]i), and that application of the Piezo1 antagonist, GsMTx4, completely blocked this change. We discovered that high and prolonged shear stress caused sustained [Ca2+]i elevation which was blocked by inhibition of TRPV4 channel opening.  Moreover, Piezo1 stimulated TRPV4 opening through activation of phospholipase A2.  TRPV4-dependent sustained [Ca2+]i elevation was responsible for fluid shear stress- and Piezo1-mediated disruption of adherens junctions and actin remodeling.  Blockade of TRPV4 channels with the selective TRPV4 blocker, HC067047, prevented the loss of endothelial cell integrity and actin disruption induced by Yoda1 or shear stress and prevented Piezo1-induced monocyte adhesion to endothelial cell monolayers.  These findings demonstrate that Piezo1 activation by fluid shear stress initiates a calcium signal that causes TRPV4 opening which in turn is responsible for the sustained phase calcium elevation that triggers pathological events in endothelial cells.  Thus, deleterious effects of shear stress are initiated by Piezo1 but require TRPV4.

The Dynamic Response of Vascular Endothelial Cells to Fluid Shear Stress

1981 ◽  
Vol 103 (3) ◽  
pp. 177-185 ◽  
Author(s):  
C. F. Dewey ◽  
S. R. Bussolari ◽  
M. A. Gimbrone ◽  
P. F. Davies
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Endothelial Cell ◽  
Dynamic Response ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cells ◽  
Shear Stresses ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Cell Functions

We have developed an in-vitro system for studying the dynamic response of vascular endothelial cells to controlled levels of fluid shear stress. Cultured monolayers of bovine aortic endothelial cells are placed in a cone-plate apparatus that produces a uniform fluid shear stress on replicate samples. Subconfluent endothelial cultures continuously exposed to 1–5 dynes/cm2 shear proliferate at a rate comparable to that of static cultures and reach the same saturation density (≃ 1.0–1.5 × 105 cells/cm2). When exposed to a laminar shear stress of 5–10 dynes/cm2, confluent monolayers undergo a time-dependent change in cell shape from polygonal to ellipsoidal and become uniformly oriented with flow. Regeneration of linear “wounds” in confluent monolayer appears to be influenced by the direction of the applied force. Preliminary studies indicate that certain endothelial cell functions, including fluid endocytosis, cytoskeletal assembly and nonthrombogenic surface properties, also are sensitive to shear stress. These observations suggest that fluid mechanical forces can directly influence endothelial cell structure and function. Modulation of endothelial behavior by fluid shear stresses may be relevant to normal vessel wall physiology, as well as the pathogenesis of vascular diseases, such as atherosclerosis.

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