Mechanosensitivity of bone cells to oscillating fluid flow induced shear stress may be modulated by chemotransport

2003 ◽  
Vol 36 (9) ◽  
pp. 1363-1371 ◽  
Author(s):  
T.L.Haut Donahue ◽  
T.R. Haut ◽  
C.E. Yellowley ◽  
H.J. Donahue ◽  
C.R. Jacobs
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Bone Cells

scholarly journals The Effect of Fluid Flow Shear Stress and Substrate Stiffness on Yes-Associated Protein (YAP) Activity and Osteogenesis in Murine Osteosarcoma Cells

Cancers ◽  
2021 ◽  
Vol 13 (13) ◽  
pp. 3128
Author(s):  
Thomas R. Coughlin ◽  
Ali Sana ◽  
Kevin Voss ◽  
Abhilash Gadi ◽  
Upal Basu-Roy ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Bone Cells ◽  
Bone Cancer ◽  
Substrate Stiffness ◽  
Flow Shear ◽  
Fluid Movement ◽  
Flow Shear Stress ◽  
Fluid Flow Shear Stress ◽  
New Treatments

Osteosarcoma (OS) is an aggressive bone cancer originating in the mesenchymal lineage. Prognosis for metastatic disease is poor, with a mortality rate of approximately 40%; OS is an aggressive disease for which new treatments are needed. All bone cells are sensitive to their mechanical/physical surroundings and changes in these surroundings can affect their behavior. However, it is not well understood how OS cells specifically respond to fluid movement, or substrate stiffness—two stimuli of relevance in the tumor microenvironment. We used cells from spontaneous OS tumors in a mouse engineered to have a bone-specific knockout of pRb-1 and p53 in the osteoblast lineage. We silenced Sox2 (which regulates YAP) and tested the effect of fluid flow shear stress (FFSS) and substrate stiffness on YAP expression/activity—which was significantly reduced by loss of Sox2, but that effect was reversed by FFSS but not by substrate stiffness. Osteogenic gene expression was also reduced in the absence of Sox2 but again this was reversed by FFSS and remained largely unaffected by substrate stiffness. Thus we described the effect of two distinct stimuli on the mechanosensory and osteogenic profiles of OS cells. Taken together, these data suggest that modulation of fluid movement through, or stiffness levels within, OS tumors could represent a novel consideration in the development of new treatments to prevent their progression.

Measurement of Osteocyte Deformation Resulting From Fluid Flow Induced Shear Stress

1999 ◽  
Author(s):  
Daniel P. Nicolella ◽  
Eugene Sprague ◽  
Lynda Bonewald
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Flow Rate ◽  
Bone Cells ◽  
Individual Cell ◽  
Analysis Techniques ◽  
Sheer Stress ◽  
Increased Sensitivity ◽  
Cell Strains ◽  
Substrate Strain

Abstract It has been shown that bone cells are more responsive to fluid flow induced shear stress as compared to applied substrate strain (Owan, et al., 1997, Smalt, et al., 1997). Using novel micromechanical analysis techniques, we have measured individual cell strains resulting from 10 minutes of continuous fluid flow at a flow rate that produces a shear stress of 15 dyne/cm2. Individual cell strains varied widely from less than 1.0% to over 25% strain within the same group of cells. The increased sensitivity of cells to fluid flow induced shear stress may be attributed to much greater cellular deformations resulting from fluid flow induced sheer stress.

Induction of NO and prostaglandin E2 in osteoblasts by wall-shear stress but not mechanical strain

1997 ◽  
Vol 273 (4) ◽  
pp. E751-E758 ◽  
Author(s):  
R. Smalt ◽  
F. T. Mitchell ◽  
R. L. Howard ◽  
T. J. Chambers
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Wall Shear Stress ◽  
Bone Cells ◽  
Mechanical Strain ◽  
Osteoblastic Cells ◽  
Long Bone ◽  
Shear Stresses ◽  
No Production ◽  
Wall Shear

The nature of the stimulus sensed by bone cells during mechanical usage has not yet been determined. Because nitric oxide (NO) and prostaglandin (PG) production appear to be essential early responses to mechanical stimulation in vivo, we used their production to compare the responsiveness of bone cells to strain and fluid flow in vitro. Cells were incubated on polystyrene film and subjected to unidirectional linear strains in the range 500–5,000 microstrain (με). We found no increase in NO or PGE2 production after loading of rat calvarial or long bone cells, MC3T3-E1, UMR-106–01, or ROS 17/2.8 cells. In contrast, exposure of osteoblastic cells to increased fluid flow induced both PGE2 and NO production. Production was rapidly induced by wall-shear stresses of 148 dyn/cm2 and was observed in all the osteoblastic populations used but not in rat skin fibroblasts. Fluid flow appeared to act through an increase in wall-shear stress. These data suggest that mechanical loading of bone is sensed by osteoblastic cells through fluid flow-mediated wall-shear stress rather than by mechanical strain.

scholarly journals A fluid–structure interaction model to characterize bone cell stimulation in parallel-plate flow chamber systems

2013 ◽  
Vol 10 (81) ◽  
pp. 20120900 ◽  
Author(s):  
T. J. Vaughan ◽  
M. G. Haugh ◽  
L. M. McNamara
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Parallel Plate ◽  
Bone Cells ◽  
Mechanical Stimulus ◽  
Flow Chamber ◽  
Parallel Plate Flow Chamber ◽  
Structure Interaction

Bone continuously adapts its internal structure to accommodate the functional demands of its mechanical environment and strain-induced flow of interstitial fluid is believed to be the primary mediator of mechanical stimuli to bone cells in vivo. In vitro investigations have shown that bone cells produce important biochemical signals in response to fluid flow applied using parallel-plate flow chamber (PPFC) systems. However, the exact mechanical stimulus experienced by the cells within these systems remains unclear. To fully understand this behaviour represents a most challenging multi-physics problem involving the interaction between deformable cellular structures and adjacent fluid flows. In this study, we use a fluid–structure interaction computational approach to investigate the nature of the mechanical stimulus being applied to a single osteoblast cell under fluid flow within a PPFC system. The analysis decouples the contribution of pressure and shear stress on cellular deformation and for the first time highlights that cell strain under flow is dominated by the pressure in the PPFC system rather than the applied shear stress. Furthermore, it was found that strains imparted on the cell membrane were relatively low whereas significant strain amplification occurred at the cell–substrate interface. These results suggest that strain transfer through focal attachments at the base of the cell are the primary mediators of mechanical signals to the cell under flow in a PPFC system. Such information is vital in order to correctly interpret biological responses of bone cells under in vitro stimulation and elucidate the mechanisms associated with mechanotransduction in vivo .

Osteoblasts respond to pulsatile fluid flow with short-term increases in PGE2 but no change in mineralization

2001 ◽  
Vol 90 (5) ◽  
pp. 1849-1854 ◽  
Author(s):  
E. A. Nauman ◽  
R. L. Satcher ◽  
T. M. Keaveny ◽  
B. P. Halloran ◽  
D. D. Bikle
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Fluid Shear Stress ◽  
Bone Cells ◽  
Shear Stresses ◽  
Long Term Effects ◽  
Fluid Shear ◽  
Short Term

Although there is no consensus as to the precise nature of the mechanostimulatory signals imparted to the bone cells during remodeling, it has been postulated that deformation-induced fluid flow plays a role in the mechanotransduction pathway. In vitro, osteoblasts respond to fluid shear stress with an increase in PGE2production; however, the long-term effects of fluid shear stress on cell proliferation and differentiation have not been examined. The goal of this study was to apply continuous pulsatile fluid shear stresses to osteoblasts and determine whether the initial production of PGE2 is associated with long-term biochemical changes. The acute response of bone cells to a pulsatile fluid shear stress (0.6 ± 0.5 Pa, 3.0 Hz) was characterized by a transient fourfold increase in PGE2 production. After 7 days of static culture (0 dyn/cm2) or low (0.06 ± 0.05 Pa, 0.3 Hz) or high (0.6 ± 0.5 Pa, 3.0 Hz) levels of pulsatile fluid shear stress, the bone cells responded with an 83% average increase in cell number, but no statistical difference ( P > 0.53) between the groups was observed. Alkaline phosphatase activity per cell decreased in the static cultures but not in the low- or high-flow groups. Mineralization was also unaffected by the different levels of applied shear stress. Our results indicate that short-term changes in PGE2 levels caused by pulsatile fluid flow are not associated with long-term changes in proliferation or mineralization of bone cells.

The influence of magnetic field on wall shear stress in power law fluid flow of blood

2021 ◽  
Author(s):  
Amira Husni Talib ◽  
Ilyani Abdullah ◽  
Nik Nabilah Nik Mohd Naser
Keyword(s):  
Magnetic Field ◽  
Shear Stress ◽  
Fluid Flow ◽  
Wall Shear Stress ◽  
Power Law ◽  
Power Law Fluid ◽  
Wall Shear

scholarly journals Endothelial Barrier Function is co-regulated at Vessel Bifurcations by Fluid Forces and Sphingosine-1-Phosphate

2020 ◽  
Author(s):  
Ehsan Akbari ◽  
Griffin B. Spychalski ◽  
Miles M. Menyhert ◽  
Kaushik K. Rangharajan ◽  
Shaurya Prakash ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Barrier Function ◽  
Endothelial Barrier ◽  
Laminar Shear Stress ◽  
Endothelial Barrier Function ◽  
Fluid Forces ◽  
Sphingosine 1 Phosphate ◽  
Laminar Shear ◽  
Vessel Bifurcations

AbstractSphingosine-1-phosphate (S1P) is a blood-borne bioactive lipid mediator of endothelial barrier function. Prior studies have implicated mechanical stimulation due to intravascular laminar shear stress in co-regulating S1P signaling in endothelial cells (ECs). Yet, vascular networks in vivo consist of vessel bifurcations, and this geometry produces hemodynamic forces that are distinct from laminar shear stress. However, the role of these forces at vessel bifurcations in regulating S1P-dependent endothelial barrier function is not known. In this study, we implemented a microfluidic platform that recapitulates the flow dynamics of vessel bifurcations with in situ quantification of the permeability of microvessel analogues. Co-application of S1P with impinging bifurcated fluid flow, which was characterized by approximately zero shear stress and 38 dyn cm-2 stagnation pressure at the vessel bifurcation point, promotes vessel stabilization. Similarly, co-treatment of carrier-free S1P with 3 dyn cm-2 laminar shear stress is also protective of endothelial barrier function. Moreover, it is shown that vessel stabilization due to laminar shear stress, but not bifurcated fluid flow, is dependent on S1P receptor 1 or 2 signaling. Collectively, these findings demonstrate the endothelium-protective function of fluid forces at vessel bifurcations and their involvement in coordinating S1P-dependent regulation of vessel permeability.

scholarly journals FLUID FLOW AND WALL SHEAR STRESS PROFILES IN MODEL BRANCH OF ABDOMINAL AORTA

Biomechanisms ◽  
1992 ◽  
Vol 11 (0) ◽  
pp. 99-109 ◽  
Author(s):  
Takashi HIROSE ◽  
Akio TANABE ◽  
Kazuo TANISHITA
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Wall Shear Stress ◽  
Abdominal Aorta ◽  
Stress Profiles ◽  
Wall Shear

scholarly journals Competing Fluid Forces Control Endothelial Sprouting in a 3-D Microfluidic Vessel Bifurcation Model

Micromachines ◽  
2019 ◽  
Vol 10 (7) ◽  
pp. 451 ◽  
Author(s):  
Ehsan Akbari ◽  
Griffin B. Spychalski ◽  
Kaushik K. Rangharajan ◽  
Shaurya Prakash ◽  
Jonathan W. Song
Keyword(s):  
Shear Stress ◽  
Fluid Flow ◽  
Bifurcation Point ◽  
Flow Dynamics ◽  
Laminar Shear Stress ◽  
Local Flow ◽  
Fluid Forces ◽  
Sprouting Angiogenesis ◽  
Laminar Shear

Sprouting angiogenesis—the infiltration and extension of endothelial cells from pre-existing blood vessels—helps orchestrate vascular growth and remodeling. It is now agreed that fluid forces, such as laminar shear stress due to unidirectional flow in straight vessel segments, are important regulators of angiogenesis. However, regulation of angiogenesis by the different flow dynamics that arise due to vessel branching, such as impinging flow stagnation at the base of a bifurcating vessel, are not well understood. Here we used a recently developed 3-D microfluidic model to investigate the role of the flow conditions that occur due to vessel bifurcations on endothelial sprouting. We observed that bifurcating fluid flow located at the vessel bifurcation point suppresses the formation of angiogenic sprouts. Similarly, laminar shear stress at a magnitude of ~3 dyn/cm2 applied in the branched vessels downstream of the bifurcation point, inhibited the formation of angiogenic sprouts. In contrast, co-application of ~1 µm/s average transvascular flow across the endothelial monolayer with laminar shear stress induced the formation of angiogenic sprouts. These results suggest that transvascular flow imparts a competing effect against bifurcating fluid flow and laminar shear stress in regulating endothelial sprouting. To our knowledge, these findings are the first report on the stabilizing role of bifurcating fluid flow on endothelial sprouting. These results also demonstrate the importance of local flow dynamics due to branched vessel geometry in determining the location of sprouting angiogenesis.

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