scholarly journals Effect of fluid shear stress on in vitro cultured ureteric bud cells

2018 ◽  
Vol 12 (4) ◽  
pp. 044107 ◽  
Author(s):  
Hiroshi Kimura ◽  
Masaki Nishikawa ◽  
Naomi Yanagawa ◽  
Hiroko Nakamura ◽  
Shunsuke Miyamoto ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Ureteric Bud ◽  
Fluid Shear

scholarly journals Turbulent fluid shear stress induces vascular endothelial cell turnover in vitro.

1986 ◽  
Vol 83 (7) ◽  
pp. 2114-2117 ◽  
Author(s):  
P. F. Davies ◽  
A. Remuzzi ◽  
E. J. Gordon ◽  
C. F. Dewey ◽  
M. A. Gimbrone
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Vascular Endothelial Cell ◽  
Vascular Endothelial ◽  
Cell Turnover ◽  
Fluid Shear ◽  
Turbulent Fluid

scholarly journals ShearFAST: a user-friendly in vitro toolset for high throughput, inexpensive fluid shear stress experiments.

2020 ◽  
Author(s):  
Thomas Brendan Smith ◽  
Alessandro Marco De Nunzio ◽  
Kamlesh Patel ◽  
Haydn Munford ◽  
Tabeer Alam ◽  
...  
Keyword(s):  
Shear Stress ◽  
High Throughput ◽  
Fluid Shear Stress ◽  
Tracking System ◽  
Frequency Measurement ◽  
Camera Motion ◽  
Fluid Shear ◽  
Mean Frequency

Fluid shear stress is a key modulator of cellular physiology in vitro and in vivo, but its effects are under-investigated due to requirements for complicated induction methods. Herein we report the validation of ShearFAST; a smartphone application that measures the rocking profile on a standard laboratory cell rocker and calculates the resulting shear stress arising in tissue culture plates. The accuracy with which this novel approach measured rocking profiles was validated against a graphical analysis, and also against measures reported by an 8-camera motion tracking system. ShearFASTs angle assessments correlated well with both analyses (r ≥0.99, p ≤0.001) with no significant differences in pitch detected across the range of rocking angles tested. Rocking frequency assessment by ShearFAST also correlated well when compared to the two independent validatory techniques (r ≥0.99, p ≤0.0001), with excellent reproducibility between ShearFAST and video analysis (mean frequency measurement difference of 0.006 ± 0.005Hz) and motion capture analysis (mean frequency measurement difference of 0.008 ± 0.012Hz). These data make the ShearFAST assisted cell rocker model make it an attractive approach for economical, high throughput fluid shear stress experiments. Proof of concept data presented reveals a protective effect of low-level shear stress on renal proximal tubule cells submitted to simulations of pretransplant storage.

Physiological fluid shear stress causes downregulation of endothelin-1 mRNA in bovine aortic endothelium

1992 ◽  
Vol 263 (2) ◽  
pp. C389-C396 ◽  
Author(s):  
A. Malek ◽  
S. Izumo
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Fluid Velocity ◽  
Low Frequency ◽  
Turbulent Shear ◽  
Specific Response ◽  
Dependent Manner ◽  
Fluid Shear ◽  
Endothelin 1

We report here that the level of endothelin-1 (ET-1) mRNA from bovine aortic endothelial cells grown in vitro is rapidly (within 1 h of exposure) and significantly (fivefold) decreased in response to fluid shear stress of physiological magnitude. The downregulation of ET-1 mRNA occurs in a dose-dependent manner that exhibits saturation above 15 dyn/cm2. The decrease is complete prior to detectable changes in endothelial cell shape and is maintained throughout and following alignment in the direction of blood flow. Peptide levels of ET-1 secreted into the media are also reduced in response to fluid shear stress. Cyclical stretch experiments demonstrated no changes in ET-1 mRNA, while increasing media viscosity with dextran showed that the downregulation is a specific response to shear stress and not to fluid velocity. Although both pulsatile and turbulent shear stress of equal time-average magnitude elicited the same decrease in ET-1 mRNA as steady laminar shear (15 dyn/cm2), low-frequency reversing shear stress did not result in any change. These results show that the magnitude as well as the dynamic character of fluid shear stress can modulate expression of ET-1 in vascular endothelium.

Nanoparticle localization in blood vessels: dependence on fluid shear stress, flow disturbances, and flow-induced changes in endothelial physiology

Nanoscale ◽  
2018 ◽  
Vol 10 (32) ◽  
pp. 15249-15261 ◽  
Author(s):  
M. Juliana Gomez-Garcia ◽  
Amber L. Doiron ◽  
Robyn R. M. Steele ◽  
Hagar I. Labouta ◽  
Bahareh Vafadar ◽  
...  
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Nanoparticle Distribution ◽  
Flow Models ◽  
Flow Disturbances ◽  
Induced Changes ◽  
Stress Flow

Hemodynamic factors drive nanoparticle distribution in vivo and in vitro in cell-based flow models.

scholarly journals In vitro generated extracellular matrix and fluid shear stress synergistically enhance 3D osteoblastic differentiation

2006 ◽  
Vol 103 (8) ◽  
pp. 2488-2493 ◽  
Author(s):  
N. Datta ◽  
Q. P. Pham ◽  
U. Sharma ◽  
V. I. Sikavitsas ◽  
J. A. Jansen ◽  
...  
Keyword(s):  
Extracellular Matrix ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Osteoblastic Differentiation ◽  
Fluid Shear

Podocytes are sensitive to fluid shear stress in vitro

2006 ◽  
Vol 291 (4) ◽  
pp. F856-F865 ◽  
Author(s):  
Colin Friedrich ◽  
Nicole Endlich ◽  
Wilhelm Kriz ◽  
Karlhans Endlich
Keyword(s):  
Shear Stress ◽  
Tyrosine Kinases ◽  
Fluid Shear Stress ◽  
Focal Adhesions ◽  
Fluid Shear ◽  
Cell Contacts ◽  
Tk Inhibitors ◽  
Static Conditions ◽  
Cell Cell

Podocytes are exposed to mechanical forces arising from glomerular capillary pressure and filtration. It has been shown that stretch affects podocyte biology in vitro and plays a significant role in the development of glomerulosclerosis in vivo. However, whether podocytes are sensitive to fluid shear stress is completely unknown. In the present study, we therefore exposed cells of a recently generated conditionally immortalized mouse podocyte cell line to defined fluid shear stress in a flow chamber, mimicking flow of the glomerular ultrafiltrate over the surface of podocytes in Bowman's space. Shear stress above 0.25 dyne/cm2 resulted in dramatic loss of podocytes but not of proximal tubular epithelial cells (LLC-PK1 cells) after 20 h. At 0.015–0.25 dyne/cm2, lamellipodia formation in podocytes was enhanced and the actin nucleation protein cortactin was redistributed to the cell margins. Shear stress further diminished stress fibers and the presence of vinculin in focal adhesions. Linear zonula occludens-1 distribution at cell-cell contacts remained unaffected at low shear stress. At 0.25 dyne/cm2, the monolayer was broken up and remaining cell-cell contacts were reinforced by F-actin and α-actinin. Because the cytoskeletal changes induced by shear stress suggested the involvement of tyrosine kinases (TKs), we tested several TK inhibitors that were all without effect on podocyte number under static conditions. At 0.25 dyne/cm2, however, the TK inhibitors genistein and AG 82 were associated with marked podocyte loss. Our data demonstrate that podocytes are highly sensitive to fluid shear stress. Shear stress induces a reorganization of the actin cytoskeleton and activates specific tyrosine kinases that are required to withstand fluid shear stress.

scholarly journals CD44 regulates blood-brain barrier integrity in response to fluid shear stress

2020 ◽  
Author(s):  
Brandon J. DeOre ◽  
Paul P. Partyka ◽  
Fan Fan ◽  
Peter A. Galie
Keyword(s):  
Blood Flow ◽  
Shear Stress ◽  
Blood Brain Barrier ◽  
Fluid Shear Stress ◽  
Small Gtpase ◽  
Brain Barrier ◽  
Fluid Shear ◽  
Blood Brain

AbstractFluid shear stress is an important mediator of vascular permeability, yet the molecular mechanisms underlying the response of the blood-brain barrier to shear have yet to be studied in cerebral vasculature despite its importance for brain homeostasis. The goal of this study is to probe components of shear mechanotransduction within the blood-brain barrier to gain a better understanding of pathologies associated with changes in cerebral blood flow including ischemic stroke. Interrogating the effects of shear stress in vivo is complicated by the complexity of factors in the brain parenchyma and the difficulty associated with modulating blood flow regimes. Recent advances in the ability to mimic the in vivo microenvironment using three-dimensional in vitro models provide a controlled setting to study the response of the blood-brain barrier to shear stress. The in vitro model used in this study is compatible with real-time measurement of barrier function using transendothelial electrical resistance as well as immunocytochemistry and dextran permeability assays. These experiments reveal that there is a threshold level of shear stress required for barrier formation and that the composition of the extracellular matrix, specifically the presence of hyaluronan, dictates the flow response. Gene editing to modulate the expression of CD44, a receptor for hyaluronan that previous studies have identified to be mechanosensitive, demonstrates that the receptor is required for the endothelial response to shear stress. Manipulation of small GTPase activity reveals CD44 activates Rac1 while inhibiting RhoA activation. Additionally, adducin-γ localizes to tight junctions in response to shear stress and RhoA inhibition and is required to maintain the barrier. This study identifies specific components of the mechanosensing complex associated with the blood-brain barrier response to fluid shear stress, and therefore illuminates potential targets for barrier manipulation in vivo.

scholarly journals PGC1α Regulates the Endothelial Response to Fluid Shear Stress via Telomerase Reverse Transcriptase Control of Heme Oxygenase-1

2021 ◽  
Author(s):  
Shashi Kant ◽  
Khanh-Van Tran ◽  
Miroslava Kvandova ◽  
Amada D. Caliz ◽  
Hyung-Jin Yoo ◽  
...  
Keyword(s):  
Shear Stress ◽  
Reverse Transcriptase ◽  
Heme Oxygenase ◽  
Fluid Shear Stress ◽  
Heme Oxygenase 1 ◽  
Telomerase Reverse Transcriptase ◽  
Fluid Shear ◽  
Flow Alignment

Fluid shear stress (FSS) is known to mediate multiple phenotypic changes in the endothelium. Laminar FSS (undisturbed flow) is known to promote endothelial alignment to flow that is key to stabilizing the endothelium and rendering it resistant to atherosclerosis and thrombosis. The molecular pathways responsible for endothelial responses to FSS are only partially understood. Here we have identified peroxisome proliferator gamma coactivator-1α (PGC-1α) as a flow-responsive gene required for endothelial flow alignment in vitro and in vivo. Compared to oscillatory FSS (disturbed flow) or static conditions, laminar FSS (undisturbed flow) increased PGC-1α expression and its transcriptional co-activation. PGC-1α was required for laminar FSS-induced expression of telomerase reverse transcriptase (TERT) in vitro and in vivo via its association with ERRα and KLF4 on the TERT promoter. We found that TERT inhibition attenuated endothelial flow alignment, elongation, and nuclear polarization in response to laminar FSS in vitro and in vivo. Among the flow-responsive genes sensitive to TERT status was heme oxygenase-1 (HMOX1), a gene required for endothelial alignment to laminar FSS. Thus, these data suggest an important role for a PGC-1α-TERT-HMOX1 axis in the endothelial stabilization response to laminar FSS.

scholarly journals Latrophilins are essential for endothelial junctional fluid shear stress mechanotransduction

2020 ◽  
Author(s):  
Keiichiro Tanaka ◽  
Andrew Prendergast ◽  
Jared Hintzen ◽  
Abhishek Kumar ◽  
Minhwan Chung ◽  
...  
Keyword(s):  
Shear Stress ◽  
G Proteins ◽  
Fluid Shear Stress ◽  
Affinity Purification ◽  
Cell Junctions ◽  
Heterotrimeric G Proteins ◽  
Fluid Shear ◽  
Vascular Morphogenesis ◽  
Flow Activation

AbstractEndothelial cell (EC) responses to fluid shear stress (FSS) are crucial for vascular development, adult physiology and disease. PECAM1 is an important transducer but earlier events remain poorly understood. We therefore investigated heterotrimeric G proteins in FSS sensing. Knockdown (KD) in ECs of single Gα proteins had little effect but combined depletion of Gαi and Gαq/11 blocked all known PECAM1-dependent responses. Re-expression of Gαi2 and Gαq but not Gαi1 and Gαi3 rescued these effects. Sequence alignment and mutational studies identified that K307 in Gαi2 and Gq/11 (Q306 in Gαi1/3), determines participation in flow signaling. We developed pull-down assays for measuring Gα activation and found that this residue, localized to the GPCR interface, determines activation by FSS. We developed a protocol for affinity purification of GPCRs on activated Gα’s, which identified latrophilins (ADGRLs) as specific upstream interactors for Gαi2 and Gq/11. Depletion of latrophilin-2 blocked EC activation of Gαi2 and Gαq, downstream events in vitro, and flow-dependent vascular morphogenesis in zebrafish embryos. Surprisingly, latrophilin-2 depletion also blocked flow activation of two additional pathways activated at cell-cell junctions, Smad1/5 and Notch1, independently of Gα proteins. Latrophilins are thus central mediators of junctional shear stress mechanotransduction via Gα protein-dependent and -independent mechanisms.

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