Concentration of soluble vascular cell adhesion molecule-1 (VCAM-1) correlated with expression of VCAM-1 mRNA in the human atherosclerotic aorta.

BACKGROUND

Adherence of circulating monocytes and lymphocytes to arterial endothelium is detectable early in experimental and human atherosclerotic plaque formation. The purpose of the present study was to assess vascular cell adhesion molecule-1 (VCAM-1) mRNA expression and the properties of soluble VCAM-1 in patients with atherosclerotic aortic disease.

METHODS

Thirteen patients with aortic disease (mean age 64 years) and 40 healthy volunteers (mean age 32 years) were included in the study. We investigated the expression of VCAM-1 mRNA in eight human aortic specimens obtained during surgery. Of these, two showed no evidence of atherosclerotic plaque formation [aortic dissection (n = 1) and annuloaortic ectasia (n = 1)], whereas six had demonstrable complex atherosclerotic formation [abdominal aneurysm (n = 5) and aortic dissection (n = 1)]. The RNase protection assay was performed using an alpha 32P-labeled 121 base pair VCAM-1 cRNA probe. We also measured concentrations of the soluble VCAM-1 using two-site enzyme immunoassays in 40 healthy volunteers and in 13 patients with abdominal and thoracic aortic aneurysms.

RESULTS

In human samples, VCAM-1 mRNA expression was found to be higher in the six patients with complex atherosclerotic formation [optical density (OD), 0.71 +/- 0.14] than in the two patients with no evidence of atherosclerotic plaque formation (OD, 0.53 and 0.49). The concentration of serum soluble VCAM-1 was higher (850 +/- 298 ng/ml) in patients with aortic or thoracic disease than in the healthy volunteers (494 +/- 94 ng/ml). In addition, there was a relationship between VCAM-1 mRNA expression and the concentration of soluble VCAM-1 (y = 2088x-554, r2 = 0.73).

CONCLUSION

VCAM-1 expression is higher in the human aorta in patients with atheromatous changes. Furthermore, concentrations of soluble VCAM-1 may provide important information about endothelial activation or in-vivo damage.