Modeling of shear stress experienced by endothelial cells cultured on microstructured polymer substrates in a parallel plate flow chamber

2011 ◽  
Vol 108 (5) ◽  
pp. 1148-1158 ◽  
Author(s):  
Alan Brown ◽  
George Burke ◽  
Brian J. Meenan
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Parallel Plate Flow Chamber ◽  
Polymer Substrates ◽  
Cells Cultured

scholarly journals A Modified Parallel Plate Flow Chamber to Study Local Endothelial Response to Recirculating Disturbed Flow

2019 ◽  
Vol 142 (4) ◽  
Author(s):  
Jason Matthew Sedlak ◽  
Alisa Morss Clyne
Keyword(s):  
Nitric Oxide ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Monocyte Adhesion ◽  
Parallel Plate Flow Chamber ◽  
Disturbed Flow ◽  
Recirculating Flow ◽  
Flow Device

Abstract Atherosclerosis develops at arterial sites where endothelial cells (ECs) are exposed to low time-averaged shear stress, in particular in regions of recirculating disturbed flow. To understand how hemodynamics contributes to EC dysfunction in atheroma development, an in vitro parallel plate flow chamber gasket was modified with protruding baffles to produce large recirculating flow regions. Computational fluid dynamics (CFD) predicted that more than 60% of the flow surface area was below the 12 dynes/cm2 atheroprotective threshold. Bovine aortic endothelial cells (BAECs) were then seeded in the parallel plate flow chamber with either the standard laminar or the new disturbed flow gasket (DFG) and exposed to flow for 36 h. Cell morphology, nitric oxide (NO), proliferation, permeability, and monocyte adhesion were assessed by phase contrast and confocal microscopy. BAEC exposed to 20 dynes/cm2 shear stress in the laminar flow device aligned and elongated in the flow direction while increasing nitric oxide, decreasing permeability, and maintaining low proliferation and monocyte adhesion. BAEC in the recirculating flow and low shear stress disturbed flow device regions did not elongate or align, produced less nitric oxide, and showed higher proliferation, permeability, and monocyte adhesion than cells in the laminar flow device. However, cells in disturbed flow device regions exposed to atheroprotective shear stress did not consistently align or decrease permeability, and these cells demonstrated low nitric oxide levels. The new parallel plate DFG provides a means to study recirculating flow, highlighting the complex relationship between hemodynamics and endothelial function.

Wall Shear Stress Determination in a Small-Scale Parallel Plate Flow Chamber Using Laser Doppler Velocimetry Under Laminar, Pulsatile and Low-Reynolds Number Turbulent Flows

2018 ◽  
Vol 140 (6) ◽  
Author(s):  
Hamed Avari ◽  
Kem A. Rogers ◽  
Eric Savory
Keyword(s):  
Shear Stress ◽  
Wall Shear Stress ◽  
Laser Doppler Velocimetry ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Laser Doppler ◽  
Small Scale ◽  
Doppler Velocimetry ◽  
Flow Conditions ◽  
Parallel Plate Flow Chamber

The parallel plate flow chamber (PPFC) has gained popularity due to its applications in fields such as biological tissue engineering. However, most of the studies using PPFC refer to theoretical relations for estimating the wall shear stress (WSS) and, hence, the accuracy of such quantifications remains elusive for anything other than steady laminar flow. In the current study, a laser Doppler velocimetry (LDV) method was used to quantify the flow in a PPFC (H = 1.8 mm × W = 17.5 mm, Dh = 3.26 mm, aspect ratio = 9.72) under steady Re = 990, laminar pulsatile (carotid Re0-mean = 282 as well as a non-zero-mean sinusoidal Re0-mean = 45 pulse) and low-Re turbulent Re = 2750 flow conditions. A mini-LDV probe was applied, and the absolute location of the LDV measuring volume with the respect to the wall was determined using a signal monitoring technique with uncertainties being around ±27 μm. The uniformity of the flow across the span of the channel, as well as the WSS assessment for all the flow conditions, was measured with the uncertainties all being less than 16%. At least two points within the viscous sublayer of the low-Re turbulent flow were measured (with the y+ for the first point < 3) and the WSS was determined using two methods with the differences between the two methods being within 5%. This paper for the first time presents the experimental determination of WSS using LDV in a small-scale PPFC under various flow conditions, the challenges associated with each condition, and a comparison between the cases. The present data will be useful for those conducting biological or numerical modeling studies using such devices.

scholarly journals MicroRNA-128 Confers Anti-Endothelial Adhesion and Anti-Migration Properties to Counteract Highly Metastatic Cervical Cancer Cells’ Migration in a Parallel-Plate Flow Chamber

2020 ◽  
Vol 22 (1) ◽  
pp. 215
Author(s):  
Pei-Chin Chuang ◽  
Chun-Wun Lu ◽  
Ching-Chin Tsai ◽  
Shun-Hung Tseng ◽  
Wen-Hong Su
Keyword(s):  
Cervical Cancer ◽  
Endothelial Cells ◽  
Cancer Cells ◽  
Parallel Plate ◽  
Flow Chamber ◽  
Caski Cell ◽  
Parallel Plate Flow Chamber ◽  
Cervical Cancer Cells ◽  
Vascular Adhesion

Despite the distant metastasis of cervical cancer cells being a prominent cause of mortality, neither the metastasis capacity nor the in vitro conditions mimicking adhesion of cervical cancer cells to endothelial cells have been fully elucidated. Circulating metastatic cancer cells undergo transendothelial migration and invade normal organs in distant metastasis; however, the putative molecular mechanism remains largely uncertain. In this study, we describe the use of an in vitro parallel-plate flow chamber to simulate the dynamic circulation stress on cervical cancer cells and elucidate their vascular adhesion and metastasis. We isolate the viable and shear stress-resistant (SSR) cervical cancer cells for mechanistic studies. Remarkably, the identified SSR-HeLa and SSR-CaSki exhibited high in vitro adhesive and metastatic activities. Hence, a consistently suppressed miR-128 level was revealed in SSR cell clones compared to those of parental wild-type (WT) cells. Overexpressed miR-128 attenuated SSR-HeLa cells’ adherence to human umbilical cord vein endothelial cells (HUVECs); in contrast, suppressed miR-128 efficiently augmented the static adhesion capacity in WT-HeLa and WT-CaSki cells. Hence, amplified miR-128 modestly abolished in vitro SSR-augmented HeLa and CaSki cell movement, whereas reduced miR-128 aggravated the migration speed in a time-lapse recording assay in WT groups. Consistently, the force expression of miR-128 alleviated the SSR-enhanced HeLa and CaSki cell mobility in a wound healing assay. Notably, miR-128 mediated SSR-enhanced HeLa and CaSki cells’ adhesion and metastasis through suppressed ITGA5, ITGB5, sLex, CEACAM-6, MMP9, and MMP23 transcript levels. Our data provide evidence suggesting that miR-128 is a promising microRNA that prevented endothelial cells’ adhesion and transendothelial migration to contribute to the SSR-enhanced adhesion and metastasis progression under a parallel-plate flow chamber system. This indicates that the nucleoid-based miR-128 strategy may be an attractive therapeutic strategy to eliminate tumor cells resistant to circulation shear flow, prevent vascular adhesion, and preclude subsequent transendothelial metastasis.

Temporal gradients in shear, but not spatial gradients, stimulate ERK1/2 activation in human endothelial cells

2005 ◽  
Vol 289 (6) ◽  
pp. H2350-H2355 ◽  
Author(s):  
Charles R. White ◽  
Hazel Y. Stevens ◽  
Mark Haidekker ◽  
John A. Frangos
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Umbilical Vein ◽  
Flow Chamber ◽  
Sudden Expansion ◽  
Endothelial Cell Proliferation ◽  
Parallel Plate Flow Chamber ◽  
Spatial Gradients ◽  
Extracellular Signal ◽  
Umbilical Vein Endothelial Cells

We have previously demonstrated temporal gradients in shear stress stimulate endothelial cell proliferation, whereas spatial gradients do not. In the present study, the extracellular signal-regulated kinases 1 and 2 (ERK1/2) pathway was investigated as a possible mediator for the promitogenic effect of temporal gradients. The sudden expansion flow chamber (SEFC) model was used to differentiate the effect of temporal gradients in shear from that of spatial gradients on ERK1/2 activation in human umbilical vein endothelial cells (HUVEC). ERK1/2 activation in the SEFC was not significantly different from control when HUVEC were exposed to spatial gradients alone. When a single temporal impulse was superimposed on spatial gradients, ERK1/2 activation was stimulated 330% (relative to spatial alone) within the region of spatial gradients. Inhibition of the ERK1/2 pathway with U-0126 abolished all effects of temporal gradients. To further separate temporal and spatial gradients, a conventional parallel plate flow chamber was utilized. Acute exposure to oscillations in flow at a frequency of 1 Hz stimulated ERK1/2 activation 620 ± 88% relative to control, whereas a single impulse of flow increased ERK1/2 activation 166 ± 19%. Flow without the temporal component did not significantly activate ERK1/2. These results suggest that the ERK1/2 pathway directly mediates the promitogenic effects of temporal gradients in shear stress.

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