OBJECTIVE: In vitro studies investigating the role of the synovial endothelium in the pathogenesis of rheumatoid arthritis (RA) have, until recently, been performed using cultured endothelial cells of nonsynovial macrovascular origin. In an attempt to more correctly model in vivo conditions, a method for the isolation and culture of synovial microvascular endothelial cells (SMEC) has been developed. METHODS: SMEC were isolated, primarily, by the use of lectin-coated (Ulex europaeus agglutinin type I), magnetizable polystyrene beads. RESULTS: Isolated cells exhibit classic endothelial "cobblestone" morphology, express von Willebrand factor, metabolize acetylated low-density lipoprotein, and exhibit a cytokine (interleukin-1)-mediated expression of endothelial leukocyte adhesion molecule type 1 (ELAM-1) and intercellular adhesion molecule type 1 (ICAM-1). ELAM-1 levels were significantly elevated in SMEC, compared with human umbilical vein endothelial cells, over a range of interleukin-1 concentrations. CONCLUSION: This increased expression of ELAM-1 by SMEC may be a potentiating step in the pathogenesis of RA.
OBJECTIVE: In vitro studies investigating the role of the synovial endothelium in the pathogenesis of rheumatoid arthritis (RA) have, until recently, been performed using cultured endothelial cells of nonsynovial macrovascular origin. In an attempt to more correctly model in vivo conditions, a method for the isolation and culture of synovial microvascular endothelial cells (SMEC) has been developed. METHODS: SMEC were isolated, primarily, by the use of lectin-coated (Ulex europaeus agglutinin type I), magnetizable polystyrene beads. RESULTS: Isolated cells exhibit classic endothelial "cobblestone" morphology, express von Willebrand factor, metabolize acetylated low-density lipoprotein, and exhibit a cytokine (interleukin-1)-mediated expression of endothelial leukocyte adhesion molecule type 1 (ELAM-1) and intercellular adhesion molecule type 1 (ICAM-1). ELAM-1 levels were significantly elevated in SMEC, compared with human umbilical vein endothelial cells, over a range of interleukin-1 concentrations. CONCLUSION: This increased expression of ELAM-1 by SMEC may be a potentiating step in the pathogenesis of RA.