scholarly journals Role of fluid shear stress in regulating VWF structure, function and related blood disorders

Biorheology ◽  
2016 ◽  
Vol 52 (5-6) ◽  
pp. 319-335 ◽  
Author(s):  
Shobhit Gogia ◽  
Sriram Neelamegham
Keyword(s):  
Shear Stress ◽  
Structure Function ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Blood Disorders

Role of cadherins and plakoglobin in interendothelial adhesion under resting conditions and shear stress

1997 ◽  
Vol 273 (5) ◽  
pp. H2396-H2405 ◽  
Author(s):  
Hans-Joachim Schnittler ◽  
Bernd Püschel ◽  
Detlev Drenckhahn
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Time Course ◽  
Fluid Shear Stress ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Platelet Endothelial Cell Adhesion ◽  
Cell Adhesion Molecule 1 ◽  
Arterial Endothelial Cells

The role of cadherins and the cadherin-binding cytosolic protein plakoglobin in intercellular adhesion was studied in cultured human umbilical venous endothelial cells exposed to fluid shear stress. Extracellular Ca2+depletion (<10−7 M) caused the disappearance of both cadherins and plakoglobin from junctions, whereas the distribution of platelet endothelial cell adhesion molecule 1 (PECAM-1) remained unchanged. Cells stayed fully attached to each other for several hours in low Ca2+ but began to dissociate under flow conditions. At the time of recalcification, vascular endothelial (VE) cadherin and β-catenin became first visible at junctions, followed by plakoglobin with a delay of ∼20 min. Full fluid shear stress stability of the junctions correlated with the time course of the reappearance of plakoglobin. Inhibition of plakoglobin expression by microinjection of antisense oligonucleotides did not interfere with the junctional association of VE-cadherin, PECAM-1, and β-catenin. The plakoglobin-deficient cells remained fully attached to each other under resting conditions but began to dissociate in response to flow. Shear stress-induced junctional dissociation was also observed in cultures of plakoglobin-depleted arterial endothelial cells of the porcine pulmonary trunk. These observations show that interendothelial adhesion under hydrodynamic but not resting conditions requires the junctional location of cadherins associated with plakoglobin. β-Catenin cannot functionally compensate for the junctional loss of plakoglobin, and PECAM-1-mediated adhesion is not sufficient for monolayer integrity under flow.

Pattern formation of vascular smooth muscle cells subject to nonuniform fluid shear stress: role of PDGF-β receptor and Src

2003 ◽  
Vol 285 (3) ◽  
pp. H1081-H1090 ◽  
Author(s):  
Shu Q. Liu ◽  
Christopher Tieche ◽  
Dalin Tang ◽  
Paul Alkema
Keyword(s):  
Shear Stress ◽  
Smooth Muscle ◽  
Cell Density ◽  
Fluid Shear Stress ◽  
Density Gradients ◽  
Dependent Manner ◽  
Fluid Shear ◽  
Polymer Implants ◽  
Β Receptor

Blood vessels are subject to fluid shear stress, a hemodynamic factor that inhibits the mitogenic activities of vascular cells. The presence of nonuniform shear stress has been shown to exert graded suppression of cell proliferation and induces the formation of cell density gradients, which in turn regulate the direction of smooth muscle cell (SMC) migration and alignment. Here, we investigated the role of platelet-derived growth factor (PDGF)-β receptor and Src in the regulation of such processes. In experimental models with vascular polymer implants, SMCs migrated from the vessel media into the neointima of the implant under defined fluid shear stress. In a nonuniform shear model, blood shear stress suppressed the expression of PDGF-β receptor and the phosphorylation of Src in a shear level-dependent manner, resulting in the formation of mitogen gradients, which were consistent with the gradient of cell density as well as the alignment of SMCs. In contrast, uniform shear stress in a control model elicited an even influence on the activity of mitogenic molecules without modulating the uniformity of cell density and did not significantly influence the direction of SMC alignment. The suppression of the PDGF-β receptor tyrosine kinase and Src with pharmacological substances diminished the gradients of mitogens and cell density and reduced the influence of nonuniform shear stress on SMC alignment. These observations suggest that PDGF-β receptor and Src possibly serve as mediating factors in nonuniform shear-induced formation of cell density gradients and alignment of SMCs in the neointima of vascular polymer implants.

Role of Cbfa1/Runx2 in the fluid shear stress induction of COX-2 in osteoblasts

2006 ◽  
Vol 341 (4) ◽  
pp. 1225-1230 ◽  
Author(s):  
Meenal Mehrotra ◽  
Masatomo Saegusa ◽  
Olga Voznesensky ◽  
Carol Pilbeam
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Fluid Shear ◽  
Stress Induction ◽  
Cox 2

Role of actin filaments in endothelial cell-cell adhesion and membrane stability under fluid shear stress

2001 ◽  
Vol 442 (5) ◽  
pp. 675-687 ◽  
Author(s):  
Hans-Joachim Schnittler ◽  
Stefan Schneider ◽  
Hartmann Raifer ◽  
Fei Luo ◽  
Peter Dieterich ◽  
...  
Keyword(s):  
Shear Stress ◽  
Cell Adhesion ◽  
Endothelial Cell ◽  
Actin Filaments ◽  
Fluid Shear Stress ◽  
Membrane Stability ◽  
Fluid Shear ◽  
Cell Cell

Role of p120-catenin in the morphological changes of endothelial cells exposed to fluid shear stress

2010 ◽  
Vol 398 (3) ◽  
pp. 426-432 ◽  
Author(s):  
Naoya Sakamoto ◽  
Kei Segawa ◽  
Makoto Kanzaki ◽  
Toshiro Ohashi ◽  
Masaaki Sato
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Morphological Changes ◽  
Fluid Shear ◽  
P120 Catenin

ROLE OF CELL-CELL JUNCTIONS IN MEDIATING ENDOTHELIAL CELL RESPONSES TO FLUID SHEAR STRESS

2004 ◽  
Vol 13 (3) ◽  
pp. 41
Author(s):  
Eleni Tzima ◽  
Mohamed Irani-Tehrani ◽  
Elizabetta Dejana ◽  
Martin Schwartz
Keyword(s):  
Shear Stress ◽  
Endothelial Cell ◽  
Fluid Shear Stress ◽  
Cell Junctions ◽  
Fluid Shear ◽  
Cell Responses ◽  
Cell Cell

scholarly journals Fluid shear stress modulates endothelial inflammation by targeting LIMS2

2020 ◽  
Vol 245 (18) ◽  
pp. 1656-1663
Author(s):  
Junyao Wang ◽  
Shiyanjin Zhang
Keyword(s):  
Shear Stress ◽  
Fluid Shear Stress ◽  
Inflammatory Factors ◽  
Zinc Finger Domain ◽  
Human Endothelial Cells ◽  
Fluid Shear ◽  
Endothelial Inflammation

Mechanosensitive genes regulate multiple cardiovascular pathophysiological processes and disorders; however, the role of flow-sensitive genes in atherosclerosis is still unknown. In this study, we identify LIM Zinc Finger Domain Containing 2 (LIMS2) that acts as a mechanosensitive gene downregulated by disturbed flow (d-flow) both in human endothelial cells (ECs) in vitro and in mice in vivo. Mechanistically, d-flow suppresses LIMS2 expression, which leads to endothelial inflammation by upregulating typical inflammatory factors, VCAM-1, and ICAM-1 in human ECs. The findings indicate that LIMS2, the new flow-sensitive gene, may help us to find a new insight to explain how d-flow caused endothelial inflammation and provide a new therapeutic approach for atherosclerosis in the future.

scholarly journals The Mechanosensory Role of Primary Cilia in Vascular Hypertension

2011 ◽  
Vol 2011 ◽  
pp. 1-9 ◽  
Author(s):  
Surya M. Nauli ◽  
Xingjian Jin ◽  
Beerend P. Hierck
Keyword(s):  
Shear Stress ◽  
Primary Cilia ◽  
Fluid Shear Stress ◽  
Vascular System ◽  
Vascular Endothelial Cells ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Cellular Functions ◽  
Continuous Problem

Local regulation of vascular tone plays an important role in cardiovascular control of blood pressure. Aside from chemical or hormonal regulations, this local homeostasis is highly regulated by fluid-shear stress. It was previously unclear how vascular endothelial cells were able to sense fluid-shear stress. The cellular functions of mechanosensory cilia within vascular system have emerged recently. In particular, hypertension is insidious and remains a continuous problem that evolves during the course of polycystic kidney disease (PKD). The basic and clinical perspectives on primary cilia are discussed with regard to the pathogenesis of hypertension in PKD.

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