Synergistic Effects of Fluid Shear Stress and Cyclic Circumferential Stretch on Vascular Endothelial Cell Morphology and Cytoskeleton

Zhao, Shuai; Suciu, Andreas; Ziegler, Thierry; Moore, James E.; Bürki, E.; Meister, Jean-Jacques; Brunner, Hans R.

doi:10.1161/01.atv.15.10.1781

Cited by 185 publications

(123 citation statements)

References 27 publications

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“…The nonspecific K ϩ channel blocker tetraethylammonium ion (TEA) has been shown to inhibit the shear stress induced increases in e-NOS and TGF-␤ 1 mRNA and cGMP concentrations in cultured endothelial cells. Synergistic effects of shear stress and cyclic circumferential stress also have been demonstrated, particularly with respect to the formation of stress fibers and F-actin organization in cultured endothelial cells (6). In other experiments, distinctive responses to cyclic strain and shear stress have been observed.…”

Section: Introductionmentioning

confidence: 75%

Circumferential deformation and shear stress induce differential responses in saphenous vein endothelium exposed to arterial flow.

Golledge¹,

Turner²,

Harley³

et al. 1997

J. Clin. Invest.

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Adaptation of saphenous vein to the hemodynamic stresses of the arterial circulation is critical to the maturation of vein bypass grafts. We have investigated early adaptive responses of venous endothelium by placing excised human saphenous vein in a bypass circuit with either venous or arterial flow conditions, using external stenting to resolve the effects of longitudinal (shear) from circumferential stress. Endothelial protein concentrations were assessed by immunostaining area (ratio of protein/CD31) and Western blotting of endothelial cell lysates (staining ratio protein/vWf).In both unstented and stented veins nitric oxide synthase increased after 90 min of arterial flow: twofold increase of immunostaining area ( P ϭ 0.001), four-to fivefold increase by Western blotting ( P ϭ 0.02), and increased A23187-mediated maximum endothelium-dependent relaxation of vein rings ( P ϭ 0.01). In unstented veins, ICAM-1 concentration was increased after 45 min of arterial flow: twofold increase by immunostaining ( P ϭ 0.001) and Western blotting ( P ϭ 0.038), with maximum fibrinogen-mediated endothelium-dependent relaxation increasing from 55.9 Ϯ 4.9 to 97 Ϯ 2.1% ( P ϭ 0.01). In contrast, in unstented veins there was a threefold decrease of VCAM-1 and no change in P-selectin after arterial flow for 45 and 90 min, respectively. However, no changes in ICAM-1 and VCAM-1 were observed in stented veins. The flow-induced alterations in nitric oxide synthase, ICAM-1, and VCAM-1 were abolished when 3 mM tetraethylammonium ion (K ϩ channel blocker) was included in the vein perfusate.The very rapid changes in ICAM-1 and VCAM-1 expression are a response to circumferential stress, whereas the slower upregulation of nitric oxide synthase is a response to longitudinal (shear) stress. Similar changes could influence the adhesiveness of endothelium in newly implanted saphenous vein bypass grafts. ( J. Clin. Invest. 1997. 99:2719-2726.)

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Section: Introductionmentioning

confidence: 75%

Circumferential deformation and shear stress induce differential responses in saphenous vein endothelium exposed to arterial flow.

Golledge¹,

Turner²,

Harley³

et al. 1997

J. Clin. Invest.

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“…Shear-induced signaling cascades and changes in endothelial cell morphology have been reviewed extensively (20,21,55). Shear stress can induce changes in endothelial cell proliferation (92), membrane fluidity (9), and cell morphology (62,96).…”

Section: Techniques For Mechanically Probing Cellsmentioning

confidence: 99%

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Huang

Kamm²,

Lee³

2004

American Journal of Physiology-Cell Physiology

487

367

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not only a complex biochemical environment but also a diverse biomechanical environment. How cells respond to variations in mechanical forces is critical in homeostasis and many diseases. The mechanisms by which mechanical forces lead to eventual biochemical and molecular responses remain undefined, and unraveling this mystery will undoubtedly provide new insight into strengthening bone, growing cartilage, improving cardiac contractility, and constructing tissues for artificial organs. In this article we review the physical bases underlying the mechanotransduction process, techniques used to apply controlled mechanical stresses on living cells and tissues to probe mechanotransduction, and some of the important lessons that we are learning from mechanical stimulation of cells with precisely controlled forces.cytoskeleton; micromanipulation; cell signaling ALL LIVING ORGANISMS face mechanical forces, from the fluid forces around a bacterium to the high forces in a human knee during stair climbing. The process of converting physical forces into biochemical signals and integrating these signals into the cellular responses is referred to as mechanotransduction. Although this review cannot cover all that has been discovered about mechanotransduction, we discuss the molecule-and cell-level structures that may participate in mechanotransduction, provide an overview of prominent techniques currently used for exerting mechanical stresses on cells, and conclude with an overview of the tissue-level response to mechanical signaling. FORCE TRANSDUCTION PATHWAYS AND SIGNALINGForce transmission pathways at the cellular and subcellular scales. Understanding the molecular basis for mechanotransduction requires knowledge of the magnitude and distribution of forces throughout the cell at the molecular scale. At present, we have sufficient information to measure molecular scale forces in only a very few cases. We can, however, analyze the mechanisms by which force is transmitted throughout the cell and use that as a basis for speculation about the molecular mechanisms of mechanotransduction. A variety of different methods have been used to mechanically stimulate a cell, and the cellular response is multifaceted and diverse. Similarly, there are likely to be a variety of sensing mechanisms and locations within the cell where forces can be transduced from a mechanical to a biochemical signal. Despite this apparent complexity, it is probable that cells stimulated in different ways are activated by similar mechanisms at the molecular level. To identify these commonalities, it is useful to consider how externally applied forces are transmitted into and throughout the cell, as well as the magnitudes and distribution of force corresponding to these different methods of stimulation.Both continuum and microstructural approaches have been used to determine force distributions. In the case of a continuum model, the details of the microstructure are ignored, and the forces transmitted via the individual microstructural elements are described in...

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“…Adult vessel physiology is directly affected by mechanotransduction of the circulation, and ECs are very sensitive to the impaired blood flow that results from atherosclerotic plaques and thromboses (29,31). We therefore assessed blood vessel integrity and function in adult mice by injecting Evans blue (EB) dye into the tail vein and then monitoring the appearance of dye in various tissues 1 hour later.…”

Section: Introductionmentioning

confidence: 99%

Lack of Protein S in mice causes embryonic lethal coagulopathy and vascular dysgenesis

Burstyn‐Cohen¹,

Heeb²,

Lemke³

2009

J. Clin. Invest.

148

170

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Protein S (ProS) is a blood anticoagulant encoded by the Pros1 gene, and ProS deficiencies are associated with venous thrombosis, stroke, and autoimmunity. These associations notwithstanding, the relative risk that reduced ProS expression confers in different disease settings has been difficult to assess without an animal model. We have now described a mouse model of ProS deficiency and shown that all Pros1 -/-mice die in utero, from a fulminant coagulopathy and associated hemorrhages. Although ProS is known to act as a cofactor for activated Protein C (aPC), plasma from Pros1 +/-heterozygous mice exhibited accelerated thrombin generation independent of aPC, and Pros1 mutants displayed defects in vessel development and function not seen in mice lacking protein C. Similar vascular defects appeared in mice in which Pros1 was conditionally deleted in vascular smooth muscle cells. Mutants in which Pros1 was deleted specifically in hepatocytes, which are thought to be the major source of ProS in the blood, were viable as adults and displayed less-severe coagulopathy without vascular dysgenesis. Finally, analysis of mutants in which Pros1 was deleted in endothelial cells indicated that these cells make a substantial contribution to circulating ProS. These results demonstrate that ProS is a pleiotropic anticoagulant with aPC-independent activities and highlight new roles for ProS in vascular development and homeostasis.

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Synergistic Effects of Fluid Shear Stress and Cyclic Circumferential Stretch on Vascular Endothelial Cell Morphology and Cytoskeleton

Cited by 185 publications

References 27 publications

Circumferential deformation and shear stress induce differential responses in saphenous vein endothelium exposed to arterial flow.

Circumferential deformation and shear stress induce differential responses in saphenous vein endothelium exposed to arterial flow.

Cell mechanics and mechanotransduction: pathways, probes, and physiology

Lack of Protein S in mice causes embryonic lethal coagulopathy and vascular dysgenesis

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