Influence of a laminar steady-state fluid-imposed wall shear stress on the binding, internalization, and degradation of low-density lipoproteins by cultured arterial endothelium.

Sprague, Eugene A.; Steinbach, Bernd; Nerem, Robert M.; Schwartz, Colin J.

doi:10.1161/01.cir.76.3.648

Cited by 158 publications

(81 citation statements)

References 30 publications

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“…28 Movements of atherogenic particles over the endothelium, and vascular smooth cell proliferation, are affected by the fluid velocity and flow characteristics in the vicinity of the endothelium. 28,29 Recirculation and turbulence in the blood flow, and changes in shear stress, have been shown to result in morphological changes in the vascular endothelial cells and in intimal thickening, promoting accumulation of atherogenic particles within the endothelium. 15,29,30 Enhanced pulsatile flow has been observed to foster turbulence and recirculation, 31 and this has been proposed to be a mechanism whereby a fast HR accelerates the progression of discrete coronary stenoses in monkeys fed an atherogenic diet.…”

Section: Table 3 Heart Rate Variability and Heart Rate In Relation Tmentioning

confidence: 99%

“…28,29 Recirculation and turbulence in the blood flow, and changes in shear stress, have been shown to result in morphological changes in the vascular endothelial cells and in intimal thickening, promoting accumulation of atherogenic particles within the endothelium. 15,29,30 Enhanced pulsatile flow has been observed to foster turbulence and recirculation, 31 and this has been proposed to be a mechanism whereby a fast HR accelerates the progression of discrete coronary stenoses in monkeys fed an atherogenic diet. 9 A combination of fast HR during sleep and enhanced de novo synthesis of lipid particles observed during sleeping hours 32 may accelerate the progression of human atherosclerosis.…”

Section: Table 3 Heart Rate Variability and Heart Rate In Relation Tmentioning

confidence: 99%

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Heart Rate Variability and Progression of Coronary Atherosclerosis

Huikuri

Jokinen

Syvänne

et al. 1999

ATVB

254

144

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Abstract-Low heart rate (HR) variability is associated with increased risk of cardiovascular morbidity and mortality, but the causes and mechanisms of this association are not well known. This prospective study was designed to test the hypothesis that reduced HR variability is related to progression of coronary atherosclerosis. Average HR and HR variability were analyzed in 12-hour ambulatory ECG recordings from 265 qualified patients participating in a multicenter study to evaluate the angiographic progression of coronary artery disease in patients with prior coronary artery bypass surgery and low high-density lipoprotein cholesterol concentrations (Ͻ1.1 mmol/L). Participants were randomized to receive a placebo or gemfibrozil therapy. The progression of coronary atherosclerosis was estimated by quantitative, computer-assisted analysis of coronary artery stenoses from the baseline angiograms and from repeated angiograms performed an average of 32 months later. The progression of focal coronary atherosclerosis of the patients randomized to placebo therapy was more marked in the tertile with the lowest standard deviation of all normal to normal R-R intervals ( Key Words: coronary artery disease Ⅲ lipids Ⅲ heart period Ⅲ angiography E levated heart rate (HR) and reduced HR variability are associated with an increased risk of cardiovascular morbidity and mortality in various populations, 1-8 but the pathophysiological link between these associations is not well understood. Experimental studies on monkeys fed an atherogenic diet have demonstrated a relationship between resting HR and progression of coronary atherosclerosis, 9 -11 and there is also a strong relationship between HR and arterial stiffness, 12 but there has been little evidence of any association between HR, or its variability, and human coronary atherosclerosis.Progression of coronary artery stenoses in repeated coronary angiograms increases the risk of adverse cardiac events, suggesting that rapid progression predisposes patients to acute complications of coronary artery plaques and serves as a surrogate end point for clinical events. 13,14 Lipid-modifying therapy has been shown to prevent the progression of coronary atherosclerosis, confirming that abnormalities in plasma lipid concentrations are strongly associated with the progression of coronary artery disease and the occurrence of adverse clinical events. 14 However, lipid theory may not explain all aspects of coronary artery disease, eg, the rapid progression of discrete stenoses in specific coronary arterial regions, which is thought to result from an interplay of hemodynamic, metabolic, and hemostatic factors. [15][16][17][18] To test the hypothesis that elevated HR and reduced HR variability are associated with the progression of human coronary atherosclerosis in patients with lipid abnormalities, we studied HR and its variability, measured by ambulatory ECG, and the angiographic progression of coronary artery disease in patients with reduced HDL cholesterol concentrations.

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Section: Table 3 Heart Rate Variability and Heart Rate In Relation Tmentioning

confidence: 99%

Section: Table 3 Heart Rate Variability and Heart Rate In Relation Tmentioning

confidence: 99%

Heart Rate Variability and Progression of Coronary Atherosclerosis

Huikuri

Jokinen

Syvänne

et al. 1999

ATVB

254

144

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“…Shear stress also increases EC stiffness, presumably reflecting changes in the cytoskeleton (20). Further, exposure ofEC to a steady state shear stress of 30 dynes/em-enhances the expression ofcellular LDL receptors (25) relative to no or low shear, an effect which is mediated by an increase in the number of receptors, rather than a change-in receptor affinity. Studies currently in progress in our laboratory also indicate that shear stress activates phosphoinositide metabolism (17), providing one pathway for intracellular signal transduction.…”

Section: The Endogenous Cells Of the Arterial Wallmentioning

confidence: 98%

Cellular Mechanisms in the Response of the Arterial Wall to Injury and Repair

et al. 1989

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This synopsis emphasizes the inappropriateness of a "single stimulus-single response" approach in understanding the response of the arterial wall to injury and repair. The outcome of any injurious stimulus is a series of interactive cascades among the endogenousand exogenous cellular and non-cellular components of the arterial wall, and the cellular and non-cellular elements of the blood. Both genetic and hemodynamic factors can further influencethis response. The more prominent of the cellular and non-cellular components have beendiscussed.These include: I) the vascularendothelium, its dynamic interaction with macromolecules and formed elements of the blood, its role in the transport of plasma proteins, its influenceon the function of arterial smooth muscle cellsand the recruitment of blood-born monocytes; 2) the arterial smooth muscle cell, its role in the vasomotor function of the artery wall, arterial repair and reconstruction, metabolism of lipids and the secretion of cytokines regulating monocyte recruitment; 3) the mononuclear phagocyte, its role in arterial debridement, metabolism of modified LDLs, a precursor of the cholesteryl ester-rich foam cell, and the secretion of neutral hydrolases, bioactive lipids and cytokines; 4) lymphocytes, as mediators of the inflammatoryresponseand possibleautoimmune reactions;5)platelets, their rolesin hemostasis,thrombosis, atherogenesis, and the repair processand 6) plasma LDLs, their oxidative modification by cells of the vessel walland their roles in the injury process.The interactive processes among arterial and circulatingcomponents in both injury and repair is emphasized.

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“…By contrast, in the same chambers, mammalian cells, which need to be maintained at 35-37 °C for maximum growth, must be perfused with fresh medium every 20-40 min [45]. The requirement in some high-resolution studies to frequently replenish the media has led to the design of various chambers in which a continuous flow of fluid is maintained across the cell surface [46,47].…”

Section: The Growth or Viewing Chambermentioning

confidence: 99%

Imaging the division process in living tissue culture cells

Khodjakov

Rieder

2006

Methods

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We detail some of the pitfalls encountered when following live cultured somatic cells by light microscopy during mitosis. Principle difficulties in this methodology arise from the necessity to compromise between maintaining the health of the cell while achieving the appropriate temporal and spatial resolutions required for the study. Although the quality of the data collected from fixed cells is restricted only by the quality of the imaging system and the optical properties of the specimen, the major limiting factor when viewing live cells is radiation damage induced during illumination. We discuss practical considerations for minimizing this damage, and for maintaining the general health of the cell, while it is being followed by multi-mode or multi-dimensional light microscopy.

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Influence of a laminar steady-state fluid-imposed wall shear stress on the binding, internalization, and degradation of low-density lipoproteins by cultured arterial endothelium.

Cited by 158 publications

References 30 publications

Heart Rate Variability and Progression of Coronary Atherosclerosis

Heart Rate Variability and Progression of Coronary Atherosclerosis

Cellular Mechanisms in the Response of the Arterial Wall to Injury and Repair

Imaging the division process in living tissue culture cells

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