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Objective— The purpose of this study was to investigate the receptor requirements for enhanced IL-1β–induced secretion of nitric oxide (NO) by endothelial cells (ECs) in the presence of fibrinogen.Methods and Results— ECs were exposed to IL-1β with or without fibrinogen and NO was measured as nitrite. NO production by EC exposed to fibrinogen (0.3±0.1 μmol/L) was comparable concentration to control (0.2±0.1 μmol/L), but IL-1β significantly increased NO production (0.8±0.1 μmol/L), and the combination of both fibrinogen and IL-1β resulted in a further increase to 2.2±0.2 μmol/L (P &lt;0.002). 7E3 or LM609, antibodies to αv β3 , inhibited NO production stimulated by fibrinogen-bound IL-1β to 0.2±0.1 μmol/L (P &lt;0.001) or 0.2±0.03 μmol/L (P &lt;0.0001), respectively. These levels were comparable to control and significantly less than with IL-1β (P &lt;0.002). EC or fibroblasts exposed to both fibrinogen and IL-1β, but not vitronectin and IL-1β, demonstrated positive Western blotting for αV β3 after immunopurification with anti- IL-1R, indicating specific association between αv β3 and IL-1R. Dual immunofluorescence also revealed colocalization of αv β3 and IL-1R only when the cells were exposed to both fibrinogen and IL-1β.Conclusion— The enhanced NO production by ECs in the presence of fibrinogen-bound IL-1β requires the coordinated effects of colocalized αV β3 and IL-1R.

Endothelial Cell Activation by IL-1β in the Presence of Fibrinogen Requires α V β 3

Endothelial Cell Activation by IL-1β in the Presence of Fibrinogen Requires α _V β ₃