Effect of Combined Cyclic Stretch and Fluid Shear Stress on Endothelial Cell Morphological Responses

2005 ◽  
Vol 127 (3) ◽  
pp. 374-382 ◽  
Author(s):  
Tomas B. Owatverot ◽  
Sara J. Oswald ◽  
Yong Chen ◽  
Jeremiah J. Wille ◽  
Frank C-P Yin
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Time Course ◽  
Fluid Shear Stress ◽  
Cyclic Stretch ◽  
Mechanical Stimuli ◽  
Cell Orientation ◽  
Fluid Shear ◽  
Aortic Endothelial Cells

Endothelial cells in vivo are normally subjected to multiple mechanical stimuli such as stretch and fluid shear stress (FSS) but because each stimulus induces magnitude-dependent morphologic responses, the relative importance of each stimulus in producing the normal in vivo state is not clear. Using cultured human aortic endothelial cells, this study first determined equipotent levels of cyclic stretch, steady FSS, and oscillatory FSS with respect to the time course of cell orientation. We then tested whether these levels of stimuli were equipotent in combination with each other by imposing simultaneous cyclic stretch and steady FSS or cyclic stretch and oscillatory FSS so as to reinforce or counteract the cells’ orientation responses. Equipotent levels of the three stimuli were 2% cyclic stretch at 2%∕s, 80dynes∕cm2 steady FSS and 20±10dynes∕cm2 oscillatory FSS at 20dyne∕cm2-s. When applied in reinforcing fashion, cyclic stretch and oscillatory, but not steady, FSS were additive. Both pairs of stimuli canceled when applied in counteracting fashion. These results indicate that this level of cyclic stretch and oscillatory FSS sum algebraically so that they are indeed equipotent. In addition, oscillatory FSS is a stronger stimulus than steady FSS for inducing cell orientation. Moreover, arterial endothelial cells in vivo are likely receiving a stronger stretch than FSS stimulus.

Role of cadherins and plakoglobin in interendothelial adhesion under resting conditions and shear stress

1997 ◽  
Vol 273 (5) ◽  
pp. H2396-H2405 ◽  
Author(s):  
Hans-Joachim Schnittler ◽  
Bernd Püschel ◽  
Detlev Drenckhahn
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Time Course ◽  
Fluid Shear Stress ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Platelet Endothelial Cell Adhesion ◽  
Cell Adhesion Molecule 1 ◽  
Arterial Endothelial Cells

The role of cadherins and the cadherin-binding cytosolic protein plakoglobin in intercellular adhesion was studied in cultured human umbilical venous endothelial cells exposed to fluid shear stress. Extracellular Ca2+depletion (<10−7 M) caused the disappearance of both cadherins and plakoglobin from junctions, whereas the distribution of platelet endothelial cell adhesion molecule 1 (PECAM-1) remained unchanged. Cells stayed fully attached to each other for several hours in low Ca2+ but began to dissociate under flow conditions. At the time of recalcification, vascular endothelial (VE) cadherin and β-catenin became first visible at junctions, followed by plakoglobin with a delay of ∼20 min. Full fluid shear stress stability of the junctions correlated with the time course of the reappearance of plakoglobin. Inhibition of plakoglobin expression by microinjection of antisense oligonucleotides did not interfere with the junctional association of VE-cadherin, PECAM-1, and β-catenin. The plakoglobin-deficient cells remained fully attached to each other under resting conditions but began to dissociate in response to flow. Shear stress-induced junctional dissociation was also observed in cultures of plakoglobin-depleted arterial endothelial cells of the porcine pulmonary trunk. These observations show that interendothelial adhesion under hydrodynamic but not resting conditions requires the junctional location of cadherins associated with plakoglobin. β-Catenin cannot functionally compensate for the junctional loss of plakoglobin, and PECAM-1-mediated adhesion is not sufficient for monolayer integrity under flow.

A device for subjecting vascular endothelial cells to both fluid shear stress and circumferential cyclic stretch

1994 ◽  
Vol 22 (4) ◽  
pp. 416-422 ◽  
Author(s):  
James E. Moore ◽  
Ernst Bürki ◽  
Andreas Suciu ◽  
Shumin Zhao ◽  
Michel Burnier ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cells ◽  
Cyclic Stretch ◽  
Vascular Endothelial ◽  
Fluid Shear

scholarly journals Fluid Shear Stress Induces Heat Shock Protein 60 Expression in Endothelial Cells In Vitro and In Vivo

2000 ◽  
Vol 20 (3) ◽  
pp. 617-623 ◽  
Author(s):  
Boris-Wolfgang Hochleitner ◽  
Elisabeth-Olga Hochleitner ◽  
Peter Obrist ◽  
Thomas Eberl ◽  
Albert Amberger ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Heat Shock ◽  
Heat Shock Protein ◽  
Fluid Shear Stress ◽  
Heat Shock Protein 60 ◽  
Fluid Shear

scholarly journals Vascular remodeling is governed by a VEGFR3-dependent fluid shear stress set point

eLife ◽  
2015 ◽  
Vol 4 ◽  
Author(s):  
Nicolas Baeyens ◽  
Stefania Nicoli ◽  
Brian G Coon ◽  
Tyler D Ross ◽  
Koen Van den Dries ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Vascular Remodeling ◽  
Fluid Shear Stress ◽  
Umbilical Vein ◽  
Fluid Shear ◽  
Set Point ◽  
Vessel Remodeling ◽  
Umbilical Vein Endothelial Cells

Vascular remodeling under conditions of growth or exercise, or during recovery from arterial restriction or blockage is essential for health, but mechanisms are poorly understood. It has been proposed that endothelial cells have a preferred level of fluid shear stress, or ‘set point’, that determines remodeling. We show that human umbilical vein endothelial cells respond optimally within a range of fluid shear stress that approximate physiological shear. Lymphatic endothelial cells, which experience much lower flow in vivo, show similar effects but at lower value of shear stress. VEGFR3 levels, a component of a junctional mechanosensory complex, mediate these differences. Experiments in mice and zebrafish demonstrate that changing levels of VEGFR3/Flt4 modulates aortic lumen diameter consistent with flow-dependent remodeling. These data provide direct evidence for a fluid shear stress set point, identify a mechanism for varying the set point, and demonstrate its relevance to vessel remodeling in vivo.

Fluid shear stress modulates cytosolic free calcium in vascular endothelial cells

1992 ◽  
Vol 262 (2) ◽  
pp. C384-C390 ◽  
Author(s):  
J. Shen ◽  
F. W. Luscinskas ◽  
A. Connolly ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cells ◽  
Free Calcium ◽  
Fluid Shear ◽  
Aortic Endothelial Cells ◽  
High K ◽  
Applied Shear Stress ◽  
Agonist Concentration

Cytosolic free Ca2+ concentration ([Ca2+]i) was monitored in single and groups of fura-2-loaded bovine aortic endothelial cells (BAEC) during exposure to laminar fluid shear stress. Application of a step increase in shear stress from 0.08 to 8 dyn/cm2 to confluent BAEC monolayers resulted in a transient increase in [Ca2+]i, which attained a peak value in 15-40 s, followed by a decline to baseline within 40-80 s. The magnitude of the [Ca2+]i responses increased with applied shear stress over the range of 0.2-4 dyn/cm2 and reached a maximum at greater than 4 dyn/cm2. Transient oscillations in [Ca2+]i with gradually diminishing amplitude were observed in individual cells subjected to continuous high shear stress. Elimination of extracellular Ca2+ with ethylene glycol-bis(beta-aminoethyl ether)-N,N,N',N'-tetraacetic acid, blockade of Ca2+ entry with lanthanum, depolarization of the cell membrane with high K+, and preconditioning of BAEC in steady laminar flow had little effect on the [Ca2+]i response. In the presence of ATP or ADP, application of shear stress caused repetitive oscillations in [Ca2+]i in single BAEC, whose frequency was dependent on both agonist concentration and the magnitude of applied shear stress. However, apyrase, an ATPase and ADPase, did not inhibit the shear-induced [Ca2+]i responses in standard medium (no added ATP or ADP), suggesting that the shear-induced [Ca2+]i response is not due to ATP released by endothelial cells.

Identification of a cis -Element Regulating Transcriptional Activity in Response to Fluid Shear Stress in Bovine Aortic Endothelial Cells

Endothelium ◽  
2003 ◽  
Vol 10 (4) ◽  
pp. 267-275 ◽  
Author(s):  
Beate Fisslthaler ◽  
Kerstin Boengler ◽  
Ingrid Fleming ◽  
Wolfgang Schaper ◽  
Rudi Busse ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Transcriptional Activity ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Aortic Endothelial Cells ◽  
Cis Element ◽  
Bovine Aortic Endothelial Cells ◽  
Aortic Endothelial

A Dielectrophoretic Device for Studying Single Cell Mechanics

2009 ◽  
Author(s):  
Kavitha Rajendran ◽  
Greeshma Manomohan ◽  
Alisa Morss Clyne
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Cell Mechanics ◽  
Fluid Shear Stress ◽  
Cell Function ◽  
Vascular Diseases ◽  
Cyclic Stretch ◽  
Fluid Shear ◽  
Mechanical Environment ◽  
Pathological Conditions

Mechanics plays an important role in cell function, both in normal physiology and pathological conditions. In the vasculature, the endothelial cells that line blood vessels dynamically respond to the mechanical environment. Endothelial cells sense both fluid shear stress and cyclic stretch, and alterations in these forces may contribute to vascular diseases such as atherosclerosis.

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