Fluid shear stress induces actin polymerization in human neutrophils

Okuyama, Masaki; Ohta, Y.; Kambayashi, Jun-ichi; Monden, Morito

doi:10.1002/(sici)1097-4644(19961215)63:4<432::aid-jcb5>3.0.co;2-u

Cited by 17 publications

(5 citation statements)

References 41 publications

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“…Moreover, the organization and structure of cytoskeletal components, such as actin, can also be modified by shear stress. 73 Other studies demonstrated differences in adhesive properties of platelets between static and dynamic conditions. 74 In a previous study we have also shown similar differences for tumor cells adhesion to ECM components.…”

Section: Discussionmentioning

confidence: 99%

Focal Adhesion Kinase Regulates Metastatic Adhesion of Carcinoma Cells within Liver Sinusoids

Sengbusch

Gaßmann

Fisch

et al. 2005

The American Journal of Pathology

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Organ-specific tumor cell adhesion to extracellular matrix (ECM) components and cell migration into host organs often involve integrin-mediated cellular processes that can be modified by environmental conditions acting on metastasizing tumor cells, such as shear forces within the blood circulation. Since the focal adhesion kinase (FAK) appears to be essential for the regulation of the integrin-mediated adhesive and migratory properties of tumor cells, its role in early steps of the metastatic cascade was investigated using in vitro and in vivo approaches. Human colon and hepatocellular carcinoma cells were used to study adhesive properties under static conditions and in a parallel plate laminar flow chamber in vitro. In addition, intravital fluorescence microscopy was used to investigate early interactions between circulating tumor cells and the microvasculature of potential target organs in vivo. Shear forces caused by hydrodynamic fluid flow induced Tyr-hyperphosphorylation of FAK in cell monolayers. Reduced expression of FAK or its endogenous inhibition by FAK-related non-kinase (FRNK) interfered with early adhesion events to extracellular matrix components under flow conditions. In contrast, tumor cell adhesion to endothelial cells under these conditions was not affected. Furthermore, down-regulation of FAK inhibited metastatic cell adhesion in vivo within the liver sinusoids. In summary, FAK appears to be involved in early events of integrin-mediated adhesion of circulating carcinoma cells under fluid flow in vitro and in vivo. This kinase may take part in the establishment of definitive adhesive interactions that enable adherent tumor cells to resist fluid shear forces, resulting in an organ-specific formation of distant metastases.

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Section: Discussionmentioning

confidence: 99%

Focal Adhesion Kinase Regulates Metastatic Adhesion of Carcinoma Cells within Liver Sinusoids

Sengbusch

Gaßmann

Fisch

et al. 2005

The American Journal of Pathology

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“…This shear stress-induced actin polymerization is not observed when neutrophils are treated with anti-CD11a/CD18 or anti-ICAM-3 antibodies. In contrast, in fMLP-stimulated neutrophils actin polymerization in pseudopods is not mediated by a rise of cytosolic intracellular Ca 2++ (Okuyama et al, 1996).…”

Section: Membrane Integrin Distribution Under Fluid Shear Stressmentioning

confidence: 83%

Fluid shear stress-mediated mechanotransduction in circulating leukocytes and its defect in microvascular dysfunction

Shin

Fukuda

Schmid‐Schönbein

2021

Journal of Biomechanics

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Leukocytes (neutrophils, monocytes) in the active circulation exhibit multiple phenotypic indicators for a low level of cellular activity, like lack of pseudopods and minimal amounts of activated, cell-adhesive integrins on their surfaces. In contrast, before these cells enter the circulation in the bone marrow or when they recross the endothelium into extravascular tissues of peripheral organs they are fully activated. We review here a multifaceted mechanism mediated by fluid shear stress that can serve to deactivate leukocytes in the circulation. The fluid shear stress controls pseudopod formation via the FPR receptor, the same receptor responsible for pseudopod projection by localized actin polymerization. The bioactivity of macromolecular factors in the blood plasma that interfere with receptor stimulation by fluid flow, such as proteolytic cleavage in the extracellular domain of the receptor or the membrane actions of cholesterol, leads to a defective ability to respond to fluid shear stress by actin depolymerization. The cell reaction to fluid shear involves CD18 integrins, nitric oxide, cGMP and Rho GTPases, is attenuated in the presence of inflammatory mediators and modified by glucocorticoids. The mechanism is abolished in disease models (genetic hypertension and hypercholesterolemia) leading to an increased number of activated leukocytes in the circulation with enhanced microvascular resistance and cell entrapment. In addition to their role in binding to biochemical agonists/antagonists, membrane receptors appear to play a second role: to monitor local fluid shear stress levels. The fluid shear stress control of many circulating cell types such as lymphocytes, stem cells, tumor cells remains to be elucidated.

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“…It has been revealed that the TMCs showed increased stress fibers in response to mechanical stimulation such as cyclic mechanical stretch ( Duffy and O’reilly, 2018 ). For other cell types, the F-actin formation had also been shown to correlate closely with the shear stress ( Okuyama et al, 1996 ; Schleicher et al, 2008 ; Mu et al, 2015 ), depending on the mode and intensity of shearing ( Chen et al, 2004 ). The dynamic regulation of F-actin polymerization of TMCs in response to the shear stress may be significant for the maintenance of outflow resistance and IOP homeostasis.…”

Section: Conclusion and Discussionmentioning

confidence: 99%

Cell senescence alters responses of porcine trabecular meshwork cells to shear stress

Zhu

et al. 2022

Front. Cell Dev. Biol.

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Mechanical microenvironment and cellular senescence of trabecular meshwork cells (TMCs) are suspected to play a vital role in primary open-angle glaucoma pathogenesis. However, central questions remain about the effect of shear stress on TMCs and how aging affects this process. We have investigated the effect of shear stress on the biomechanical properties and extracellular matrix regulation of normal and senescent TMCs. We found a more significant promotion of Fctin formation, a more obvious realignment of F-actin fibers, and a more remarkable increase in the stiffness of normal cells in response to the shear stress, in comparison with that of senescent cells. Further, as compared to normal cells, senescent cells show a reduced extracellular matrix turnover after shear stress stimulation, which might be attributed to the different phosphorylation levels of the extracellular signal-regulated kinase. Our results suggest that TMCs are able to sense and respond to the shear stress and cellular senescence undermines the mechanobiological response, which may lead to progressive failure of cellular TM function with age.

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Fluid shear stress induces actin polymerization in human neutrophils

Cited by 17 publications

References 41 publications

Focal Adhesion Kinase Regulates Metastatic Adhesion of Carcinoma Cells within Liver Sinusoids

Focal Adhesion Kinase Regulates Metastatic Adhesion of Carcinoma Cells within Liver Sinusoids

Fluid shear stress-mediated mechanotransduction in circulating leukocytes and its defect in microvascular dysfunction

Cell senescence alters responses of porcine trabecular meshwork cells to shear stress

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