Design and construction of a linear shear stress flow chamber

Usami, Shunichi; Chen, Hsuan-Hsu; Zhao, Yihua; Chien, Shu; Skalak, Richard

doi:10.1007/bf02368167

Cited by 288 publications

(234 citation statements)

References 9 publications

Supporting

Mentioning

231

Contrasting

Unclassified

Order By: Relevance

“…All experiments were conducted in a parallel plate flow chamber with a tapered channel design based on the Hele-Shaw flow theory between parallel plates (39). The selectin-coated microscope slides served as the bottom plate of the flow chamber.…”

Section: Methodsmentioning

confidence: 99%

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Im¹,

Fu²,

Wang³

et al. 2004

Cancer Research

268

210

View full text Add to dashboard Cite

Coagulation has long been known to facilitate metastasis. To pinpoint the steps where coagulation might play a role in the metastasis, we used three-dimensional visualization of direct infusion of fluorescence labeled antibody to observe the interaction of tumor cells with platelets and fibrinogen in isolated lung preparations. Tumor cells arrested in the pulmonary vasculature were associated with a clot composed of both platelets and fibrin(ogen). Initially, the cells attached to the pulmonary vessels were rounded. Over the next 2 to 6 hours, they spread on the vessel surface. The associated clot was lysed coincident with tumor cell spreading. To assess the importance of clot formation, we inhibited coagulation with hirudin, a potent inhibitor of thrombin. The number of tumor cells initially arrested in the lung of hirudin-treated mice was essentially the same as in control mice. However, tumor cell spreading and subsequent retention of the tumor cells in the lung was markedly inhibited in the anticoagulated mice. These associations of the tumor cells with platelets were independent of tumor cell expression of P-selectin ligands. This work identifies tumor cell spreading onto the vascular surface as an important component of the metastatic cascade and implicates coagulation in this process.

show abstract

Section: Methodsmentioning

confidence: 99%

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Im¹,

Fu²,

Wang³

et al. 2004

Cancer Research

268

210

View full text Add to dashboard Cite

show abstract

“…In the present research, we studied the effects of a non-uniform WSS field by building a flow chamber that provides a temporally-steady but spatially-varying shear field and that covers the atherogenic (< 0.4 Pa) and atheroprotective (> 1.2 Pa) shear ranges (Malek et al, 1999) and values in between. Similar to the chamber previously proposed by Usami et al (Usami et al, 1993), our device generates a known, linearly decreasing WSS through the use of a slowly expanding flow channel. Thus, one set of measurements on a single chamber can provide a wide range of shear field measurements.…”

Section: Introductionmentioning

confidence: 92%

Role of Ultrasonic Shear Rate Estimation Errors in Assessing Inflammatory Response and Vascular Risk

Tsou

Liu

Barakat

et al. 2008

Ultrasound in Medicine & Biology

View full text Add to dashboard Cite

Atherosclerotic lesions preferentially originate in arterial regions that experience low wall shear stress (WSS) and reversing flow patterns. Therefore, routinely monitoring arterial WSS may help to identify the potential sites of early atherosclerosis. A new non-invasive ultrasonic method implemented with coded excitation techniques was utilized to improve WSS estimation accuracy and precision by providing high spatial and temporal resolution. WSS measurement errors were quantified in a model system by scanning a linearly-varying WSS field (0.3-1.9 Pa) within a flow chamber. A 13-bit Optimal code was found to be most effective in reducing bias and standard deviation in WSS estimates down to ~ 10 % and ~ 8 %. The measurement errors slowly increased with input WSS for all imaging pulses. The expression of endothelial cellular adhesion molecules VCAM-1 and E-selectin was investigated over a similar shear range (0-1.6 Pa) in order to study the impact of relating shear-mediated cellular adhesion molecule (CAM) expression to inaccuracies in WSS measurements. We quantified this influence as the prediction error, which accounts for the ultrasonic measurement errors and the sensitivity of CAM expression within certain shear ranges. The highest prediction errors were observed at WSS < 0.8 Pa, where CAM expression is most responsive to WSS. The results emphasize the importance of minimizing estimation errors, especially within low shear regions. Preliminary 2-D in vivo shear imaging is also presented to provide information about the spatial heterogeneity in arterial WSS distribution.

show abstract

“…Cell interaction with immobilized vWF under flow conditions was observed in real time by means of epifluorescence videomicroscopy in a modified Hele-Shaw flow chamber (35), as described previously (4). Purified human vWF was diluted to a final concentration of 20 g/ml with 2 mM ammonium acetate, pH 7.0, and 200 l of the protein solution was spread evenly onto a glass coverslip (No.…”

mentioning

confidence: 99%

Regulation of von Willebrand Factor Binding to the Platelet Glycoprotein Ib-IX by a Membrane Skeleton-dependent Inside-out Signal

Englund

Bodnar

et al. 2001

Journal of Biological Chemistry

View full text Add to dashboard Cite

The platelet receptor for von Willebrand factor (vWF), glycoprotein Ib-IX (GPIb-IX), mediates initial platelet adhesion and activation. We show here that the receptor function of GPIb-IX is regulated intracellularly via its link to the filamin-associated membrane skeleton. Deletion of the filamin binding site in GPIb␣ markedly enhances ristocetin-(or botrocetin)-induced vWF binding and allows GPIb-IX-expressing cells to adhere to immobilized vWF under both static and flow conditions. Cytochalasin D (CD) that depolymerizes actin also enhances vWF binding to wild type GPIb-IX. Thus, vWF binding to GPIb-IX is negatively regulated by the filamin-associated membrane skeleton. In contrast to native vWF, binding of the isolated recombinant vWF A1 domain to wild type and filamin binding-deficient mutants of GPIb-IX is comparable, suggesting that the membrane skeleton-associated GPIb-IX is in a state that prevents access to the A1 domain in macromolecular vWF. In platelets, there is a balance of membrane skeleton-associated and free forms of GPIb-IX. Treatment of platelets with CD increases the free form and enhances vWF binding. CD also reverses the inhibitory effects of prostaglandin E1 on vWF binding to GPIb-IX. Thus, GPIb-IX-dependent platelet adhesion is doubly controlled by vWF conformation and a membrane skeletondependent inside-out signal.

show abstract

Design and construction of a linear shear stress flow chamber

Cited by 288 publications

References 9 publications

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Coagulation Facilitates Tumor Cell Spreading in the Pulmonary Vasculature during Early Metastatic Colony Formation

Role of Ultrasonic Shear Rate Estimation Errors in Assessing Inflammatory Response and Vascular Risk

Regulation of von Willebrand Factor Binding to the Platelet Glycoprotein Ib-IX by a Membrane Skeleton-dependent Inside-out Signal

Contact Info

Product

Resources

About