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Vascular cell adhesion molecule-1 (VCAM-1) is transiently expressed on vascular endothelial cells in response to cytokines. It plays a major role in the adhesion of leucocytes to the endothelium by interaction with its ligand VLA-4, a member of the β1 integrin family. We measured the serum concentration of the soluble VCAM-1 (sVCAM-1) in 114 patients with acute myocardial infarction (AMI) and 37 normal controls by enzyme-linked immunoassay in comparison with trace element concentration. sVCAM-1 levels were markedly higher (mean± SD=833.2±328.9 ng/ml) in the sera of patients with AMI than in normal controls (mean±SD= 549.5±188.8 ng/ml, p<0.001). Using PIXE we also determined concentration of magnesium, manganese, iron, copper, zinc, selenium, and calcium in sera of 43 patients with AMI. There were no clear correlation between the sVCAM-1 concentration and the magnesium, manganese, copper, selenium. But there were significant correlation between the sVCAM-1 concentration and the zinc, calcium (p<0.05).

Vascular cell adhesion molecule-1 (VCAM-1) is transiently expressed on vascular endothelial cells in response to cytokines. It plays a major role in the adhesion of leucocytes to the endothelium by interaction with its ligand VLA-4, a member of the β1 integrin family.

We measured the serum concentration of the soluble VCAM-1 (sVCAM-1) in 114 patients with acute myocardial infarction (AMI) and 37 normal controls by enzyme-linked immunoassay in comparison with trace element concentration. sVCAM-1 levels were markedly higher (mean ± SD=833.2 ± 328.9 ng/ml) in the sera of patients with AMI than in normal controls (mean ± SD= 549.5 ± 188.8 ng/ml, p<0.001). Using PIXE we also determined concentration of magnesium, manganese, iron, copper, zinc, selenium, and calcium in sera of 43 patients with AMI. There were no clear correlation between the sVCAM-1 concentration and the magnesium, manganese, copper, selenium, iron. But there were significant correlation between the sVCAM-1 concentration and the zinc, calcium (p<0.05).

Vascular endothelial cells (ECs) are subjected to shear stress and cytokine stimulation. We studied the interplay between shear stress and cytokine in modulating the expression of adhesion molecule genes and the adhesive function of ECs. Shear stress (20 dynes/cm²) was applied to ECs prior to or following the addition of tumor necrosis factor (TNF)-α. Shear stress increased the TNF-α-induced expression of intercellular adhesion molecule-1 (ICAM-1) at both mRNA and surface protein levels, but decreased the TNF-α-induced expression of vascular adhesion molecule-1 (VCAM-1). The TNF-α-induced increase in EC adhesiveness for monocytic THP-1 cells was reduced by shear stress. After 24-h pre-shearing followed by 1 h of static incubation, the effect of pre-shearing on TNF-α-induced ICAM-1 mRNA expression vanished. The recovery of the TNF-α-induced VCAM-1 mRNA expression following pre-shearing, however, required a static incubation time of >6 h (completely recovery at 24 h). Pre- and post-shearing caused a reduction in the nuclear factor (NF)-κB-DNA binding activity induced by TNF-α in the EC nucleus. Our findings suggest that shear stress plays differential roles in modulating the TNF-α-induced EC expressions of ICAM-1 and VCAM-1 genes, which serve similar functions in vascular biology.