The procyanidin-induced pseudo laminar shear stress response: a new concept for the reversal of endothelial dysfunction

2004 ◽  
Vol 107 (5) ◽  
pp. 513-517 ◽  
Author(s):  
Roger CORDER ◽  
Richard C. WARBURTON ◽  
Noorafza Q. KHAN ◽  
Ruth E. BROWN ◽  
Elizabeth G. WOOD ◽  
...  
Keyword(s):  
Heart Failure ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Stress Response ◽  
Endothelial Dysfunction ◽  
Grape Seed ◽  
Similar Response ◽  
Laminar Shear Stress ◽  
Shear Stress Response ◽  
Laminar Shear

Reduced endothelium-dependent vasodilator responses with increased synthesis of ET-1 (endothelin-1) are characteristics of endothelial dysfunction in heart failure and are predictive of mortality. Identification of treatments that correct these abnormalities may have particular benefit for patients who become refractory to current regimens. Hawthorn preparations have a long history in the treatment of heart failure. Therefore we tested their inhibitory effects on ET-1 synthesis by cultured endothelial cells. These actions were compared with that of GSE (grape seed extract), as the vasoactive components of both these herbal remedies are mainly oligomeric flavan-3-ols called procyanidins. This showed extracts of hawthorn and grape seed were equipotent as inhibitors of ET-1 synthesis. GSE also produced a potent endothelium-dependent vasodilator response on preparations of isolated aorta. Suppression of ET-1 synthesis at the same time as induction of endothelium-dependent vasodilation is a similar response to that triggered by laminar shear stress. Based on these results and previous findings, we hypothesize that through their pharmacological properties procyanidins stimulate a pseudo laminar shear stress response in endothelial cells, which helps restore endothelial function and underlies the benefit from treatment with hawthorn extract in heart failure.

scholarly journals On the large difference between Benjamin’s and Hanratty’s formulations of perturbed flow over uneven terrain

2019 ◽  
Vol 871 ◽  
pp. 534-561
Author(s):  
Paolo Luchini ◽  
François Charru
Keyword(s):  
Boundary Layer ◽  
Shear Stress ◽  
Stress Response ◽  
Eddy Viscosity ◽  
Laminar Shear Stress ◽  
Uneven Terrain ◽  
Eddy Viscosity Model ◽  
Shear Stress Response ◽  
Sommerfeld Equation ◽  
Laminar Shear

Flow over an uneven terrain is a complex phenomenon that requires a chain of approximations in order to be studied. In addition to modelling the intricacies of turbulence if present, the problem is classically first linearized about a flat bottom and a locally parallel flow, and then asymptotically approximated into an interactive representation that couples a boundary layer and an irrotational region through an intermediate inviscid but rotational layer. The first of these steps produces a stationary Orr–Sommerfeld equation; since this is a one-dimensional problem comparatively easy for any computer, it would seem appropriate today to forgo the second sweep of approximation and solve the Orr–Sommerfeld problem numerically. However, the results are inconsistent! It appears that the asymptotic approximation tacitly restores some of the original problem’s non-parallelism. In order to provide consistent results, Benjamin’s version of the Orr–Sommerfeld equation needs to be modified into Hanratty’s. The large difference between Benjamin’s and Hanratty’s formulations, which arises in some wavenumber ranges but not in others, is here explained through an asymptotic analysis based on the concept of admittance and on the symmetry transformations of the boundary layer. A compact and accurate analytical formula is provided for the wavenumber range of maximum laminar shear-stress response. We highlight that the maximum turbulent shear-stress response occurs in the quasi-laminar regime at a Reynolds-independent wavenumber, contrary to the maximum laminar shear-stress response whose wavenumber scales with a power of the boundary-layer thickness. A numerical computation involving an eddy-viscosity model provides a warning against the inaccuracy of such a model. We emphasize that the range $k\unicode[STIX]{x1D708}/u_{\unicode[STIX]{x1D70F}}<10^{-3}$ of the spectrum remains essentially unexplored, and that the question is still open whether a fully developed turbulent regime, similar to the one predicted by an eddy-viscosity model, ever exists for open flow even in the limit of infinite wavelength.

scholarly journals Primary cilia of human endothelial cells disassemble under laminar shear stress

2004 ◽  
Vol 164 (6) ◽  
pp. 811-817 ◽  
Author(s):  
Carlo Iomini ◽  
Karla Tejada ◽  
Wenjun Mo ◽  
Heikki Vaananen ◽  
Gianni Piperno
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Primary Cilia ◽  
Umbilical Vein ◽  
Intraflagellar Transport ◽  
Mechanical Stimuli ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Umbilical Vein Endothelial Cells ◽  
Laminar Shear

We identified primary cilia and centrosomes in cultured human umbilical vein endothelial cells (HUVEC) by antibodies to acetyl-α-tubulin and capillary morphogenesis gene-1 product (CMG-1), a human homologue of the intraflagellar transport (IFT) protein IFT-71 in Chlamydomonas. CMG-1 was present in particles along primary cilia of HUVEC at interphase and around the oldest basal body/centriole at interphase and mitosis. To study the response of primary cilia and centrosomes to mechanical stimuli, we exposed cultured HUVEC to laminar shear stress (LSS). Under LSS, all primary cilia disassembled, and centrosomes were deprived of CMG-1. We conclude that the exposure to LSS ends the IFT in cultured endothelial cells.

Laminar shear stress promotes mitochondrial homeostasis in endothelial cells

2018 ◽  
Vol 233 (6) ◽  
pp. 5058-5069 ◽  
Author(s):  
Li-Hong Wu ◽  
Hao-Chun Chang ◽  
Pei-Ching Ting ◽  
Danny L. Wang
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Shear Stress ◽  
Mitochondrial Homeostasis ◽  
Laminar Shear

A Promoter Polymorphism Regulates NFKB1 Gene Transactivity in Human Endothelial Cells under Laminar Shear Stress

2006 ◽  
Vol 38 (Supplement) ◽  
pp. S4
Author(s):  
Joon Y. Park ◽  
Iain K. Farrance ◽  
Hanjoong Jo ◽  
Steven R. Brant ◽  
Stephen M. Roth ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Promoter Polymorphism ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Laminar Shear

AXL ACTIVATION MEDIATES LAMINAR SHEAR STRESS ANTIAPOPTOTIC EFFECTS IN HUMAN ENDOTHELIAL CELLS

2004 ◽  
Vol 13 (3) ◽  
pp. 194
Author(s):  
Daniela D'Arcangelo ◽  
Valeria Ambrosino ◽  
Gianluca Ragone ◽  
Maria Giannuzzo ◽  
Maurizio C Capogrossi ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Shear Stress ◽  
Human Endothelial Cells ◽  
Laminar Shear

Laminar shear stress inhibits CXCR4 expression on endothelial cells: functional consequences for atherogenesis

2005 ◽  
Vol 19 (6) ◽  
pp. 1-25 ◽  
Author(s):  
Roberta Melchionna ◽  
Daniele Porcelli ◽  
Antonella Mangoni ◽  
Daniele Carlini ◽  
Giovanna Liuzzo ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Cxcr4 Expression ◽  
Laminar Shear Stress ◽  
Functional Consequences ◽  
Laminar Shear

Recruitment of endothelial caveolae into mechanotransduction pathways by flow conditioning in vitro

2003 ◽  
Vol 285 (4) ◽  
pp. H1720-H1729 ◽  
Author(s):  
Victor Rizzo ◽  
Christine Morton ◽  
Natacha DePaola ◽  
Jan E. Schnitzer ◽  
Peter F. Davies
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Cell Surface ◽  
Tyrosine Phosphorylation ◽  
Surface Proteins ◽  
Luminal Surface ◽  
Laminar Shear Stress ◽  
Caveolin 1 ◽  
Cultured Endothelial Cells ◽  
Laminar Shear

The luminal surface of rat lung microvascular endothelial cells in situ is sensitive to changing hemodynamic parameters. Acute mechanosignaling events initiated in response to flow changes in perfused lung microvessels are localized within specialized invaginated microdomains called caveolae. Here we report that chronic exposure to shear stress alters caveolin expression and distribution, increases caveolae density, and leads to enhanced mechanosensitivity to subsequent changes in hemodynamic forces within cultured endothelial cells. Flow-preconditioned cells expressed a fivefold increase in caveolin (and other caveolar-residing proteins) at the luminal surface compared with no-flow controls. The density of morphologically identifiable caveolae was enhanced sixfold at the luminal cell surface of flow-conditioned cells. Laminar shear stress applied to static endothelial cultures (flow step of 5 dyn/cm2), enhanced the tyrosine phosphorylation of luminal surface proteins by 1.7-fold, including caveolin-1 by 1.3-fold, increased Ser1179 phosphorylation of endothelial nitric oxide synthase (eNOS) by 2.6-fold, and induced a 1.4-fold activation of mitogen-activated protein kinases (ERK1/2) over no-flow controls. The same shear step applied to endothelial cells preconditioned under 10 dyn/cm2 of laminar shear stress for 6 h and induced a sevenfold increase of total phosphotyrosine signal at the luminal endothelial cell surface enhanced caveolin-1 tyrosine phosphorylation 5.8-fold and eNOS phosphorylation by 3.3-fold over static control values. In addition, phosphorylated caveolin-1 and eNOS proteins were preferentially localized to caveolar microdomains. In contrast, ERK1/2 activation was not detected in conditioned cells after acute shear challenge. These data suggest that cultured endothelial cells respond to a sustained flow environment by directing caveolae to the cell surface where they serve to mediate, at least in part, mechanotransduction responses.

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