The Response of Adult Human Saphenous Vein Endothelial Cells to Combined Pressurized Pulsatile Flow and Cyclic Strain, In Vitro

Tsukurov, Olga; Kwolek, Christopher J.; L’Italien, Gilbert; Benbrahim, Aziz; Milinazzo, B.; Conroy, Nancy; Gertler, Jonathan P.; Orkin, Roslyn W.; Abbott, William M.

doi:10.1007/s100169910044

Cited by 26 publications

(18 citation statements)

References 21 publications

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“…ET-1 secretion was elevated at SPAϭϪ180°compared with SPAϭ0°as well, but that was not the condition with the highest ET-1 secretion ( Figure 3B). In an experiment in an elastic tube with Ϯ4% CS, Ϸ5Ϯ2 dynes/cm 2 , and undefined SPA (likely near 0°), Tsukurov et al 18 showed a similar decrease in ET-1 mRNA expression at 48 hours. In the present study, SS insignificantly reduced ET-1 mRNA levels compared with SC ( Figure 3A).…”

Section: Discussionmentioning

confidence: 97%

Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells

Dancu

Berardi

Heuvel

et al. 2004

ATVB

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Objective-Endothelium-derived vasoactive agents NO, endothelin-1 (ET-1), and prostacyclin (PGI 2 ) not only regulate vascular tone but also influence atherogenic processes, including smooth muscle migration and proliferation, as well as monocyte and platelet adhesion. Complex hemodynamics characterized by the temporal phase angle between mechanical factors circumferential strain and wall shear stress (stress phase angle [SPA]) have been implicated in regions prone to pathologic development, such as atherosclerosis and intimal hyperplasia, in coronary and peripheral arteries where the mechanical forces are highly asynchronous (SPAϭϪ180°). We determined the gene expression of endothelial NO synthase (eNOS), ET-1, and cyclooxygenase-2 (COX-2) affected by asynchronous hemodynamics (SPAϭϪ180°) relative to normal hemodynamics (SPAϭ0°) in bovine aortic endothelial cells. Methods and Results-Quantitative competitive RT-PCR analysis showed that eNOS production (at 5 and 12 hours) and COX-2 production (at 5 hours) were reduced at the gene expression level by asynchronous hemodynamics (SPAϭϪ180°) compared with synchronous hemodynamics (SPAϭ0°), whereas ET-1 exhibited an opposite trend (at 5 and 12 hours). NO, ET-1, and PGI 2 secretion followed their respective gene expression profiles after 5 and 12 hours. Conclusion-Together, these data suggest that highly asynchronous mechanical force patterns (SPAϭϪ180°) Key Words: hemodynamics Ⅲ shear stress and strain Ⅲ coronary arteries Ⅲ eNOS Ⅲ ET-1 Ⅲ COX-2 E ndothelial dysfunction is a primary event in development of atherosclerosis, vasospasm, and thrombosis. 1,2 Endothelium-derived vasoactive agents such as NO, endothelin-1 (ET-1), and prostacyclin (PGI 2 ) not only regulate vascular tone but also influence atherogenic processes, including smooth muscle migration and proliferation, as well as monocyte and platelet adhesion. 3 Endothelial cells (ECs) are a primary target for injuries such as hyperlipidemia, diabetes mellitus, and hypertension 2 but also serve as sensors and transducers of the most notable hemodynamic forces: wall shear stress (WSS) and circumferential stress that is induced by circumferential strain (CS [or stretch]). WSS and CS are widely believed to be important hemodynamic mediators of vascular regulation, atherosclerosis, and remodeling. 4 -7 Most previous studies of the role of vascular mechanical forces in atherogenesis have emphasized fluid shear stress (WSS) by itself (ie, no pressure or strain). 4 -7 A few recent studies have noted the importance of complex hemodynamics that include simultaneous flow, pressure, and diameter variation (stretch) in modulating cardiovascular function. 6 -9 Blood vessel ECs in vivo are subjected to simultaneous pulsatile CS and WSS that act approximately in perpendicular directions. The temporal phase angle between pressure and flow (impedance phase angle) generated by global wave reflection in the circulation and the local inertial effects of blood flow cause time lags to occur between CS and WSS. The temporal phase an...

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Section: Discussionmentioning

confidence: 97%

Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells

Dancu

Berardi

Heuvel

et al. 2004

ATVB

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“…19,20 The importance of the microenvironment in governing venous/arterial identity is further supported by cell culture studies in which flow induces an arterial phenotype in venous ECs. 21,22 Coronary artery bypass grafting provides potential insights into the plasticity of venous endothelium. When veins are grafted into the arterial circulation, they acquire arterial-like properties, including a thickened wall and, in animal models, reduced permeability.…”

Section: Arteries and Veinsmentioning

confidence: 99%

Phenotypic Heterogeneity of the Endothelium

Aird¹

2007

Circulation Research

970

736

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Abstract-Endothelial cells, which form the inner cellular lining of blood vessels and lymphatics, display remarkable heterogeneity in structure and function. This is the second of a 2-part review on the phenotypic heterogeneity of blood vessel endothelial cells. The first part discusses the scope, the underlying mechanisms, and the diagnostic and therapeutic implications of phenotypic heterogeneity. Here, these principles are applied to an understanding of organ-specific phenotypes in representative vascular beds including arteries and veins, heart, lung, liver, and kidney. The goal is to underscore the importance of site-specific properties of the endothelium in mediating homeostasis and focal vascular pathology, while at the same time emphasizing the value of approaching the endothelium as an integrated system. (Circ Res. 2007;100: 174-190.)

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“…This suggests that the ET-1 activity is controlled by the balance between the two forces. The combination of these two mechanical forces acts to neutralise the effect on ET-1 (for expression of stretch-induced genes in inflammation, see table 2) [65,66]. In addition to causing vasoconstriction, stretch-induced ET-1 mRNA from arterial ECs has been reported to affect VSMCs by increasing apoptosis [67].…”

Section: Stretch-regulated Genes Affecting the Inflammatory Response mentioning

confidence: 99%

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

et al. 2012

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High blood pressure is responsible for the modulation of blood vessel morphology and function. Arterial hypertension is considered to play a significant role in atherosclerotic ischaemic heart disease, stroke and hypertensive nephropathy, whereas high venous pressure causes varicose vein formation and chronic venous insufficiency and contributes to vein bypass graft failure. Hypertension exerts differing injurious forces on the vessel wall, namely shear stress and circumferential stretch. Morphological and molecular changes in blood vessels ascribed to elevated pressure consist of endothelial damage, neointima formation, activation of inflammatory cascades, hypertrophy, migration and phenotypic changes in vascular smooth muscle cells, as well as extracellular matrix imbalances. Differential expression of genes encoding relevant factors including vascular endothelial growth factor, endothelin-1, interleukin-6, vascular cell adhesion molecule, intercellular adhesion molecule, matrix metalloproteinase-2 and -9 and plasminogen activator inhibitor-1 has been explored using ex vivo cellular or organ stretch models and in vivo experimental animal models. Identification of pertinent genes may unravel new therapeutic strategies to counter the effects of pressure-induced stretch on the vessel wall and hence minimise its notable complications.

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The Response of Adult Human Saphenous Vein Endothelial Cells to Combined Pressurized Pulsatile Flow and Cyclic Strain, In Vitro

Cited by 26 publications

References 21 publications

Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells

Asynchronous Shear Stress and Circumferential Strain Reduces Endothelial NO Synthase and Cyclooxygenase-2 but Induces Endothelin-1 Gene Expression in Endothelial Cells

Phenotypic Heterogeneity of the Endothelium

The Effect of Pressure-Induced Mechanical Stretch on Vascular Wall Differential Gene Expression

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