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Am J Physiol Cell Physiol 276: C1100-C1107, 1999;
0363-6143/99 $5.00
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Vol. 276, Issue 5, C1100-C1107, May 1999

Regulation of low shear flow-induced HAEC VCAM-1 expression and monocyte adhesion

Sumathy Mohan1, Natarajan Mohan2, Anthony J. Valente3, and Eugene A. Sprague1

1 Division of Cardiovascular and Special Intervention and 2 Division of Radiation Oncology, Department of Radiology and 3 Department of Medicine, University of Texas Health Science Center, San Antonio, Texas 78284-7800

We recently reported that prolonged exposure of human aortic endothelial cells (HAEC) to low shear stress flow patterns is associated with a sustained increase in the activated form of the transcriptional regulator nuclear factor-kappa B (NF-kappa B). Here we investigate the hypothesis that low shear-induced activation of NF-kappa B is responsible for enhanced expression of vascular cell adhesion molecule (VCAM-1) resulting in augmented endothelial cell-monocyte (EC-Mn) adhesion and that this activation is dependent on intracellular oxidant activity. Before exposure to low shear (2 dyn/cm2) for 6 h, HAEC were preincubated with or without the antioxidants pyrrolidine dithiocarbamate (PDTC) or N-acetyl-L-cysteine (NAC). PDTC strongly inhibited low shear-induced activation of NF-kappa B, expression of VCAM-1, and EC-Mn adhesion. Paradoxically, NAC exerted a positive effect on low shear-induced VCAM-1 expression and EC-Mn adhesion and only slightly downregulated NF-kappa B activation. However, cytokine-induced NF-kappa B activation and VCAM-1 expression are blocked by both PDTC and NAC. These data suggest that NF-kappa B plays a key role in low shear-induced VCAM-1 expression and that pathways mediating low shear- and cytokine-induced EC-Mn adhesion may be differentially regulated.

transcription regulator; hemodynamics; atherosclerosis; human aortic endothelial cell; nuclear factor-kappa B; vascular cell adhesion molecule


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