Low shear stress wall slip in polymer melts : an experimental investigation

1996 ◽  
Author(s):  
David Henson
Keyword(s):  
Experimental Investigation ◽  
Shear Stress ◽  
Polymer Melts ◽  
Wall Slip ◽  
Low Shear Stress ◽  
Low Shear

Low shear stress-induced endothelial mesenchymal transformation via the down-regulation of TET2

2021 ◽  
Vol 545 ◽  
pp. 20-26
Author(s):  
AFang Li ◽  
LiLan Tan ◽  
ShuLei Zhang ◽  
Jun Tao ◽  
Zuo Wang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Down Regulation ◽  
Low Shear Stress ◽  
Mesenchymal Transformation ◽  
Low Shear

Plaque and Shear Stress Distribution in Human Coronary Bifurcations: a Multi-Slice Computed Tomography Study

2007 ◽  
Author(s):  
Alina G. van der Giessen ◽  
Jolanda J. Wentzel ◽  
Frans N. van de Vosse ◽  
Antonius F. van der Steen ◽  
Pim J. de Feyter ◽  
...  
Keyword(s):  
Computed Tomography ◽  
Shear Stress ◽  
Outer Wall ◽  
Atherosclerotic Plaques ◽  
Advanced Stage ◽  
Flow Divider ◽  
Low Shear Stress ◽  
Curved Vessels ◽  
Early Atherosclerosis ◽  
Low Shear

It is generally accepted that early atherosclerosis develops in low shear-stress (SS) regions such as the outer wall of arterial bifurcations and the inner bend of curved vessels (1). However, in clinical practice, it is common to observe atherosclerotic plaques at the flow-divider, or carina, of coronary bifurcations (2). Plaques at the carina are more frequently found in symptomatic patients, and may represent a more advanced stage of atherosclerosis. The carina is located in a region which is exposed to high SS. We hypothesize that if plaques are located in atheroprotective high SS regions, they have grown circumferentially from the atherogenic low SS regions.

CXCR4 expression in atherosclerotic lesions induced by low shear stress

2008 ◽  
Vol 32 (3) ◽  
pp. S18-S19
Author(s):  
Dang Heng Wei ◽  
Gui Xue Wang ◽  
Yi Ping Xia ◽  
Jian Jun Lei ◽  
Lu Shang Liu ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cxcr4 Expression ◽  
Atherosclerotic Lesions ◽  
Low Shear Stress ◽  
Low Shear

scholarly journals Low Shear Stress Induced HMGB1 Translocation and Release via PECAM-1/PARP-1 Pathway to Induce Inflammation Response

PLoS ONE ◽  
2015 ◽  
Vol 10 (3) ◽  
pp. e0120586 ◽  
Author(s):  
Wei-dong Qin ◽  
Shao-hua Mi ◽  
Chen Li ◽  
Gui-xia Wang ◽  
Jian-ning Zhang ◽  
...  
Keyword(s):  
Shear Stress ◽  
Inflammation Response ◽  
Low Shear Stress ◽  
Parp 1 ◽  
Low Shear

QS358. Programmed Cell Death in Low Shear Stress and Balloon Induced Arterial Restenosis

2008 ◽  
Vol 144 (2) ◽  
pp. 409-410
Author(s):  
Lisa R.P. Spiguel ◽  
Amito Chandiwal ◽  
Ralph R. Weichselbaum ◽  
Christopher L. Skelly
Keyword(s):  
Cell Death ◽  
Shear Stress ◽  
Programmed Cell Death ◽  
Arterial Restenosis ◽  
Low Shear Stress ◽  
Low Shear

scholarly journals Effects of Caveolin-1-ERK1/2 pathway on endothelial cells and smooth muscle cells under shear stress

2019 ◽  
Vol 245 (1) ◽  
pp. 21-33 ◽  
Author(s):  
Lan Jia ◽  
Lihua Wang ◽  
Fang Wei ◽  
Chen Li ◽  
Zhe Wang ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Smooth Muscle ◽  
Growth Factor ◽  
Caveolin 1 ◽  
Low Shear Stress ◽  
And Migration ◽  
Oscillating Shear Stress ◽  
Low Shear ◽  
Proliferation And Migration

Hemodynamic forces have an important role in venous intimal hyperplasia, which is the main cause of arteriovenous fistula dysfunction. Endothelial cells (ECs) constantly exposed to the shear stress of blood flow, converted the mechanical stimuli into intracellular signals, and interacted with the underlying vascular smooth muscle cells (VSMCs). Caveolin-1 is one of the important mechanoreceptors on cytomembrane, which is related to vascular abnormalities. Extracellular signal-regulated kinase1/2 (ERK1/2) pathway is involved in the process of VSMCs proliferation and migration. In the present study, we explore the effects of Caveolin-1-ERK1/2 pathway and uremia toxins on the endothelial cells and VSMCs following shear stress application. Different shear stress was simulated with a ECs/VSMCs cocultured parallel-plate flow chamber system. Low shear stress and oscillating shear stress up-regulated the expression of fibroblast growth factor-4, platelet-derived growth factor-BB, vascular endothelial growth factor-A, ERK1/2 phosphorylation in endothelial cells, and proliferation and migration of VSMCs but down-regulated the Caveolin-1 expression in endothelial cells. Uremia toxin induces the proliferation and migration of VSMCs but not in a Caveolin-1-dependent manner in the static environment. Low shear stress-induced proliferation and migration of VSMCs is inhibited by Caveolin-1 overexpression and ERK1/2 suppression. Shear stress-regulated VSMC proliferation and migration is an endothelial cells-dependent process. Low shear stress and oscillating shear stress exert atherosclerotic influences on endothelial cells and VSMCs. Low shear stress modulated proliferation and migration of VSMCs through Caveolin-1-ERK1/2 pathway, which suggested that Caveolin-1 and ERK1/2 can be used as a new therapeutic target for the treatment of arteriovenous fistula dysfunction. Impact statement Venous intimal hyperplasia is the leading cause of arteriovenous fistula (AVF) dysfunction. This article reports that shear stress-regulated vascular smooth muscle cells (VSMCs) proliferation and migration is an endothelial cell (EC)-dependent process. Low shear stress (LSS) and oscillating shear stress (OSS) exert atherosclerotic influences on the ECs and VSMCs. LSS-induced proliferation and migration of VSMCs is inhibited by Caveolin-1 overexpression and extracellular signal-regulated kinase1/2 (ERK1/2) suppression, which suggested that Caveolin-1 and ERK1/2 can be used as a new therapeutic target for the treatment of AVF dysfunction.

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