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It has been known for more than 70 years that although risk factors act over the entire vascular system, atherosclerotic plaques develop at preferred arterial sites, such as bifurcations, curved segments, and side branches, where shear stress is reduced and flow may become turbulent.
While it has long been appreciated that changes in flow-induced wall stress underlie this phenomenon, we have only recently started to gain a deeper knowledge of the cellular and molecular mechanisms involved. In this session, the speakers have given a wide-angle and stimulating view of recent research in this field, exploring the various aspects of this issue in different experimental models, from cultured endothelial cells to isolated arteries and in vivo animal models.
The first speaker, Dr. Zakrzewicz (Berlin, DE), gave a picture of the changes in endothelial gene expression induced by shear stress in vitro via the activation of mechanoceptors, which translate signals by the outside flow into the cells. Normal levels of shear stress may exert anti-atherogenic effects by reducing CD36 expression and monocyte recruitment, decreasing endothelin-1 generation, and increasing nitric oxide generation. On the other hand, changes from laminar to turbulent flow increase complement activation, and may thus favour inflammation and thrombosis.
Dr. Krams’ (Amsterdam, NL) presentation was mostly focused on in vivo effects of wall shear stress. In mice with pro-atherogenic phenotype, he evaluated the effects of reduced shear stress, with or without generation of oscillatory flow, on carotid atherogenesis. Low levels of shear stress were accompanied by plaque formation; interestingly, in the presence of flow oscillation plaques exhibited a “stable” phenotype, while low shear stress alone was accompanied by “vulnerable” plaque formation (with increased lipid and macrophage content and reduced collagen content).
Dr. Koller (Valhalla, NY, USA) explored the role of increased blood pressure in modifying vessel wall properties. In normal conditions, oxygen radicals, currently viewed as the “bad guys”, exert vasodilating action. However, when pressure is increased, oxygen radical generation also rises, with subsequent scavenging of nitric oxide and impaired vasodilation, which also translates in a pro-atherogenic phenotype of endothelial cells. Wall stress may thus alter the intracellular balance between superoxide radical and nitric oxide generation, modulating the redox state of vascular wall.
The last speaker, Dr. Weinberg (London, UK) started his lecture from the observations of Dr. Anitschkow on the location of lipid accumulation within aortic wall, dated from 1933. He then compared these very early studies with conflicting data later obtained by other investigators. In his presentation he suggested that the same arterial site might be exposed to different levels of shear stress throughout life, from young to old age.
Discussion by the audience ranged from the possible role of different flow patterns, pressure levels, and diastolic vs systolic flow, to stretch-mediated effects on vessel wall, intracellular site of radical generation, acute or chronic exposure to stimuli in the various experimental models employed, effects of age on endothelial properties, and more. The regulatory role of nitric oxide/superoxide balance within cells again seems to be an important player in the field. The large audience of the session and the stimulating discussion once more confirm that the availability of new techniques may shed a new light on old issues and give origin to new lines of research, also after 70 years.
1568 - 1571
Atherosclerosis is shear stress! Symposium - State of the Art in Basic Science
Our mission: To reduce the burden of cardiovascular disease
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