Background. β2-Microglobulin (β2m) amyloidosis is a destructive articular disease that affects patients on dialysis. The disease presentation is similar to other forms of arthritis in which adhesion molecules are felt to be pathogenic. Therefore, we hypothesized that β2m directly increases the expression of vascular cell adhesion molecule-1 (VCAM-1) by synovial fibroblasts. We also examined the effect of alteration of β2m by advanced glycation end products on this cellular response. Methods. Human synovial fibroblasts were isolated and incubated with β2m with and without alteration with advanced glycation end products. VCAM-1 expression was determined by immunohistochemistry, flow cytometry, and Western blot and Northern blot analyses. Results. β2m increased the protein expression of VCAM-1 by synovial fibroblasts in a dose-dependent manner. β2m altered with advanced glycation end products had no effect. However, all forms of β2m increased VCAM-1 mRNA. β2m also increased the adhesion of peripheral blood mononuclear cells to synovial fibroblasts. Conclusion. β2m directly increases the expression of VCAM-1 by synovial fibroblasts, indicating that synovial fibroblasts may play a key role in the pathogenesis of β2m amyloidosis.
|Original language||English (US)|
|Number of pages||9|
|State||Published - Jan 1 2001|
- Advanced glycation end products
- Articular disease
- Dialysis amyloid
ASJC Scopus subject areas