scholarly journals Fluid shear stress modulates surface expression of adhesion molecules by endothelial cells

Blood ◽  
1995 ◽  
Vol 85 (7) ◽  
pp. 1696-1703 ◽  
Author(s):  
M Morigi ◽  
C Zoja ◽  
M Figliuzzi ◽  
M Foppolo ◽  
G Micheletti ◽  
...  
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Flow ◽  
Fluid Shear Stress ◽  
Leukocyte Adhesion ◽  
Interleukin 1 ◽  
Static Condition ◽  
Surface Expression ◽  
Cell Surface Expression ◽  
Interleukin 1 Beta

We investigated the effect of hemodynamic shear forces on the expression of adhesive molecules, E-selectin, and intercellular adhesion molecule-1 (ICAM-1) on human umbilical vein endothelial cells (HUVEC) exposed to laminar (8 dynes/cm2) or turbulent shear stress (8.6 dynes/cm2 average), or to a static condition. Laminar flow induced a significant time-dependent increase in the surface expression of ICAM-1, as documented by flow cytometry studies. Endothelial cell surface expression of ICAM-1 in supernatants of HUVEC exposed to laminar flow was not modified, excluding the possibility that HUVEC exposed to laminar flow synthetize factors that upregulate ICAM-1. The effect of laminar flow was specific for ICAM-1, while E-selectin expression was not modulated by the flow condition. Turbulent flow did not affect surface expression of either E-selectin or ICAM-1. To evaluate the functional significance of the laminar-flow-induced increase in ICAM-1 expression, we studied the dynamic interaction of total leukocyte suspension with HUVEC exposed to laminar flow (8 dynes/cm2 for 6 hours) in a parallel-plate flow chamber or to static condition. Leukocyte adhesion to HUVEC pre-exposed to flow was significantly enhanced, compared with HUVEC maintained in static condition (233 +/- 67 v 43 +/- 16 leukocytes/mm2, respectively), and comparable with that of interleukin-1 beta treated HUVEC. Mouse monoclonal antibody anti-ICAM-1 completely blocked flow-induced upregulation of leukocyte adhesion. Interleukin-1 beta, which upregulated E-selectin expression, caused leukocyte rolling on HUVEC that was significantly lower on flow- conditioned HUVEC and almost absent on untreated static endothelial cells. Thus, laminar flow directly and selectively upregulates ICAM-1 expression on the surface of endothelial cells and promotes leukocyte adhesion. These data are relevant to the current understanding of basic mechanisms that govern local inflammatory reactions and tissue injury.

An Apparatus to Study the Response of Cultured Endothelium to Shear Stress

1986 ◽  
Vol 108 (4) ◽  
pp. 332-337 ◽  
Author(s):  
R. F. Viggers ◽  
A. R. Wechezak ◽  
L. R. Sauvage
Keyword(s):  
Finite Element ◽  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Flow ◽  
Fluid Shear Stress ◽  
Shear Stresses ◽  
Parallel Plates ◽  
Dimensional Flow ◽  
Wide Range ◽  
Wall Shear

An apparatus which has been developed to study the response of cultured endothelial cells to a wide range of shear stress levels is described. Controlled laminar flow through a rectangular tube was used to generate fluid shear stress over a cell-lined coverslip comprising part of one wall of the tube. A finite element method was used to calculate shear stresses corresponding to cell position on the coverslip. Validity of the finite element analysis was demonstrated first by its ability to generate correctly velocity profiles and wall shear stresses for laminar flow in the entrance region between infinitely wide parallel plates (two-dimensional flow). The computer analysis also correctly predicted values for pressure difference between two points in the test region of the apparatus for the range of flow rates used in these experiments. These predictions thus supported the use of such an analysis for three-dimensional flow. This apparatus has been used in a series of experiments to confirm its utility for testing applications. In these studies, endothelial cells were exposed to shear stresses of 60 and 128 dynes/cm2. After 12 hr at 60 dynes/cm2, cells became aligned with their longitudinal axes parallel to the direction of flow. In contrast, cells exposed to 128 dynes/cm2 required 36 hr to achieve a similar reorientation. Interestingly, after 6 hr at 128 dynes/cm2, specimens passed through an intermediate phase in which cells were aligned perpendicular to flow direction. Because of its ease and use and the provided documentation of wall shear stress, this flow chamber should prove to be a valuable tool in endothelial research related to atherosclerosis.

scholarly journals Hemodynamic shear stress characteristic of atherosclerosis-resistant regions promotes glycocalyx formation in cultured endothelial cells

2013 ◽  
Vol 304 (2) ◽  
pp. C137-C146 ◽  
Author(s):  
Andrew Koo ◽  
C. Forbes Dewey ◽  
Guillermo García-Cardeña
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Heparan Sulfate ◽  
Vascular Endothelial Cells ◽  
Surface Expression ◽  
Endothelial Glycocalyx ◽  
Cell Surface Expression ◽  
Apical Surface ◽  
Laminar Shear Stress ◽  
Critical Components

The endothelial glycocalyx, a glycosaminoglycan layer located on the apical surface of vascular endothelial cells, has been shown to be important for several endothelial functions. Previous studies have documented that the glycocalyx is highly abundant in the mouse common carotid region, where the endothelium is exposed to laminar shear stress, and it is resistant to atherosclerosis. In contrast, the glycocalyx is scarce or absent in the mouse internal carotid sinus region, an area exposed to nonlaminar shear stress and highly susceptible to atherosclerosis. On the basis of these observations, we hypothesized that the expression of components of the endothelial glycocalyx is differentially regulated by distinct hemodynamic environments. To test this hypothesis, human endothelial cells were exposed to shear stress waveforms characteristic of atherosclerosis-resistant or atherosclerosis-susceptible regions of the human carotid, and the expression of several components of the glycocalyx was assessed. These experiments revealed that expression of several components of the endothelial glycocalyx is differentially regulated by distinct shear stress waveforms. Interestingly, we found that heparan sulfate expression is increased and evenly distributed on the apical surface of endothelial cells exposed to the atheroprotective waveform and is irregularly present in cells exposed to the atheroprone waveform. Furthermore, expression of a heparan sulfate proteoglycan, syndecan-1, is also differentially regulated by the two waveforms, and its suppression mutes the atheroprotective flow-induced cell surface expression of heparan sulfate. Collectively, these data link distinct hemodynamic environments to the differential expression of critical components of the endothelial glycocalyx.

Calcium responses of endothelial cell monolayers subjected to pulsatile and steady laminar flow differ

1995 ◽  
Vol 269 (2) ◽  
pp. C367-C375 ◽  
Author(s):  
G. Helmlinger ◽  
B. C. Berk ◽  
R. M. Nerem
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Laminar Flow ◽  
Oscillatory Flow ◽  
Static Condition ◽  
Free Calcium ◽  
Aortic Endothelial Cells ◽  
Hemodynamic Forces ◽  
Intracellular Free Calcium Concentration ◽  
Free Calcium Concentration

The vascular endothelium is the primary transducer of hemodynamically imposed mechanochemical events. In this study, we measured the intracellular free calcium concentration ([Ca2+]i) using the fluorescent probe fura 2 and ratiometric digital imaging in cultured bovine aortic endothelial cells (BAEC) subjected to various laminar flow patterns. These were steady shear stress (0.2-70 dyn/cm2) and three types of sinusoidal pulsatile shear stress (nonreversing: 40 +/- 20 dyn/cm2; reversing: 20 +/- 40 dyn/cm2; and purely oscillatory: 0 +/- 20 dyn/cm2; flow frequencies: 0.4, 1.0, and 2.0 Hz) in a serum-containing medium. The most dramatic finding was failure of a purely oscillatory flow to increase [Ca2+]i in BAEC monolayers. In contrast, steady flow, as well as nonreversing and reversing pulsatile flows, increased [Ca2+]i. The dynamics of the response were dependent on the flow pattern. Both internal Ca2+ release and extracellular Ca2+ entry were involved in these [Ca2+]i increases. Also, switching from either a steady nonreversing pulsatile or reversing pulsatile flow back to a static condition resulted in a [Ca2+]i increase. However, switching from an oscillatory flow to a static condition did not induce any changes in average [Ca2+]i. This study shows that endothelial cells are able to sense different flow environments in terms of [Ca2+]i signaling and is relevant to further studies of the influence of hemodynamic forces on vascular pathophysiology.

Studying Inflammatory Responses of Endothelial Cells and Leukocytes in Perfused Microchannels

2006 ◽  
Author(s):  
Gerard B. Nash
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Inflammatory Responses ◽  
Leukocyte Adhesion ◽  
Rectangular Cross Section ◽  
Blood Stream ◽  
Shear Stresses ◽  
Immune Functions ◽  
Endothelial Genes

Circulating leukocytes must adhere to the endothelial cells (EC) that form the lining of blood vessels, and migrate through them to carry out their protective immune functions. During inflammation this recruitment is typically controlled by cytokines released from tissue that act on the EC. The endothelial cells respond by increasing the expression of adhesion molecules on their surface (to capture flowing leukocytes), and also by presenting chemotactic agents (to induce the captured cells to migrate). This recruitment process is influenced by the local haemodynamic milieu in several ways: interactions with red cells modify the distribution of leukocytes in the blood stream; flow velocity and shear stress influence the formation and breakage of adhesive bonds; flow forces act on EC and modify their responses to inflammmatory cytokines. Microchannels have been widely used to study these processes, especially the specific receptors required for capture of isolated flowing leukocytes and their ability to support adhesion as a function of fluid shear stress. We developed a versatile system based on pre-fabricated glass capillaries with rectangular cross-section (microslides) in which we cultured EC, and which could also be coated with purified adhesion receptors for reductive studies. We also developed fluoresence-microscope-based systems for using these microslides to observe adhesion in flowing whole blood, and multiple parallel cultures for studying the effects of conditioning the EC by growth at different levels of shear stress before investigations. The microslides are available in various dimensions, and smaller versions can be used to generate high circulatory stresses when small volumes of materials (such as blood from genetically modified mice) are available. With these systems, we have for instance, been able to show how varying the concentration and aggregability of red blood cells alters leukocyte adhesion, and how expression levels of endothelial genes which underly inflammatory responses are modified by culture at a range of shear stresses mimicking different regions of the circulation.

scholarly journals Lepasnya Sel Endotel Dan Vascular Endothelial Cadherin (Ve-Cadherin) Pada Huvecs Dengan Glukosa Tinggi Dan Fluid Shear Stress

2020 ◽  
Vol 8 (2) ◽  
pp. 92
Author(s):  
Yoyon Arif ◽  
Erna Sulistiowati
Keyword(s):  
Endothelial Cells ◽  
Shear Stress ◽  
Fluid Shear Stress ◽  
Vascular Endothelial ◽  
Fluid Shear ◽  
Vascular Endothelial Cadherin

Sel endotel melapisi lumen pembuluh darah sehingga menyebabkan paparan langsung aliran darah dan timbul gaya hemodinamik shear stress. Vascular Endothelial (VE) Cadherin merupakan salah satu struktur penghubung antar sel yang berperan mencegah terlepasnya sel endotel dari membran dasar. Paparan glukosa tinggi menyebabkan stress oksidatif sehingga sel endotel mengalami apoptosis dan nekrosis dan terlepas. Penelitian ini bertujuan mempelajari efek paparan glukosa tinggi dan fluid shear stress terhadap morfologi, struktur VE-Cadherin dan densitas sel endotel pada kultur sel endotel HUVECs (Human Vein Endothelial Cells Culture).Metode Penelitian eksperimental laboratorium dengan  metode HUVECs yang dipapar d-glukosa 22 mM selama 7 hari. Shear stress dibangkitkan dengan alat cone and plate 10 dyne/cm2 selama 5, 8, 12 dan 15 menit. Pulasan VE-Cadherin dengan imunohistokimia. Data dianalisis dengan metode statistik. Signifikan pada p<0,05.Hasil Shear stress selama 15 menit menyebabkan perubahan bentuk sel endotel  menjadi lebih panjang dan inti sel lebih pipih. Paparan glukosa tinggi dan fluid shear stress menyebabkan penurunan skor VE-Cadherin dan densitas sel endotel secara signifikan Penurunan skor VE-Cadherin berpengaruh langsung terhadap penurunan densitas sel endotel.Kesimpulan. Paparan glukosa tinggi dan fluid shear stress menyebabkan kerusakan struktur VE-Cadherin sehingga terjadi peningkatan apoptosis dan nekrosis sel endotel.

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