Effect of Ni ions on expression of intercellular adhesion molecule 1 by endothelial cells

✍ Scribed by Wataha, J. C. ;Sun, Z. L. ;Hanks, C. T. ;Fang, D. N.

• Publisher: John Wiley and Sons
• Year: 1997
• Tongue: English
• Weight: 149 KB
• Volume: 36
• Category: Article
• ISSN: 0021-9304
• DOI: 10.1002/(sici)1097-4636(199708)36:2<145::aid-jbm2>3.0.co;2-k

✦ Synopsis

Previous studies have shown that Ni-based alloys implanted into soft tissues cause an infiltration of inflammatory cells around the implant. This phenomenon is potentially important to dental alloys which are adjacent to oral tissues. To help define the mechanisms by which Ni causes an infiltration of inflammatory cells, we exposed endothelial cells in vitro to Ni ions and measured the expression of intercellular adhesion molecule 1 (ICAM-1). ICAM-1 is known to be involved in the recruitment of inflammatory cells from the bloodstream. We also exposed macrophages to Ni ions to test the hypothesis that Ni might alter cytokine secretion and subsequently cause expression of ICAM-1 on endothelial cells. The results showed that Ni ions could promote the expression of ICAM-1 on endothelial cells, but only at concentrations which were high enough (850 mumol/L for 24 h) to suppress cell metabolic activity. Although we had previous evidence that Ni could cause macrophages to secrete cytokines such as interleukin 1 beta, Ni-exposed macrophage supernatants did not induce expression of ICAM-1 on endothelial cells at concentrations subtoxic to the macrophages (85 mumol/L). At subtoxic concentrations, Ni ions were able to suppress ICAM-1 expression on endothelial cells which were stimulated with lipopolysaccharide. Thus, Ni ions either promoted or suppressed the expression of ICAM-1 depending on their concentration. This dual action of Ni ions may be important in vivo where a gradient of concentrations of released ions is likely to exist around the implanted biomaterial. Further studies are necessary to determine the effect of time of exposure and the molecular mechanisms of increased ICAM-1 expression.