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(Circulation Research. 2009;104:931.)
© 2009 American Heart Association, Inc.

Editorials

Extracellular Matrix Differentiating Good Flow Versus Bad Flow

John Y.-J. Shyy

From the Division of Biomedical Sciences, University of California, Riverside.

Correspondence to John Y.-J. Shyy, PhD, Division of Biomedical Sciences, University of California, Riverside, CA 92521. E-mail john.shyy@ucr.edu

See related article, pages 995–1003

Key Words: shear stress • endothelial cells • JNK

An extract of the first 250 words of the full text is provided, because this article has no abstract.

Mounting evidence indicates that shear stress, the tangential component of blood flow acting on the vessel wall, is crucial for endothelial functions and pathophysiology. From the vascular biology point of view, arterial areas under laminar flow, with high mean shear stress and little bidirectional oscillation, are atheroprotective, whereas areas under disturbed flow, with oscillation, reverse flow, and low mean shear stress, are atheroprone. This principle holds true for vessel specimens from both human patients and various animal models. To assess the effect of distinct flow patterns at the molecular level, immunocytochemical methods are commonly used to detect the expression of genes in areas experiencing laminar versus disturbed flow. For example, the expression of vascular cell adhesion molecule-1 and intercellular adhesion molecule-1, indicative of vascular inflammation, is markedly enhanced in regions prone to atherosclerosis in low-density lipoprotein receptor-null mice fed an atherogenic diet.¹

From the perspective of fluid mechanics, laminar flow has low Reynolds number and is characterized by smooth, constant fluid motion. In contrast, turbulent flow has high Reynolds number and tends to cause eddies, vortices, and other flow disturbances. Flow channels have been used as in vitro models to investigate the mechanisms by which shear stress modulates endothelial functions, because they permit close control over the fluid mechanics imposed on cultured vascular endothelial cells (ECs). Advances in molecular and cell biology, in conjunction with flow channel experiments, have facilitated investigations into the mechanotransduction mechanism by which shear stress modulates gene expression in cultured ECs. Many second-messenger systems in ECs . . . [Full Text of this Article]

Related Article:

The Subendothelial Extracellular Matrix Modulates JNK Activation by Flow

Cornelia Hahn, A. Wayne Orr, John M. Sanders, Krishna A. Jhaveri, and Martin Alexander Schwartz
Circ. Res. 2009 104: 995-1003. [Abstract] [Full Text] [PDF]