Aim To investigate the effect of fibrinogen on proliferation,chemotaxis and migration of vascular smooth muscle cell (VSMC) and to explore the possible effect and mechanism of fibrinogen in the formation of atherosclerosis. Methods Rat aorta smooth muscle cells were primarily cultured. VSMC proliferation was evaluated by BrdU incorporation assay and visual cell counting. VSMC migration and chemotaxis were measured with scrape assay,time-lapse microcinematography and Boyden's chemotaxis assay. Glutinase A expression and activity were assessed by Western blotting and zymography techniques. Results BrdU incorporation assay(r=0.880,p<0.05)and visual cell counting (r=0.860,p<0.05)showed that fibrinogen stimulated the proliferation of VSMC dose-dependently in the range between 0.2 g/L and 3.2 g/L. The cell counts of VSMC after 48 h incubation with the concentrations of fibrinogen as 0.4,0.8,1.6 and 3.2 g/L were significantly higher than control group[(6.32±0.39)×10 7 cells/L,(10.63±0.25)×10 7 cells/L,(12.31±0.44)×10 7 cells/L and (13.59±0.43)×10 7 cells/L vs.(5.63±0.34)×10 7 cells/L,(p<0.01)]. The BrdU incorporation rates of fibrinogen of 0.4, 0.8, 1.6 and 3.2 g/L were also significantly higher than control group (5.2%±2.2%,17.5%±2.0%,21.5%±2.3% and 25.5%±2.5% vs.2.0%±0.8%,p<0.01). Fibrinogen stimulated the chemotaxis of VSMC dose-dependently in the range between 0.2 g/L and 3.2 g/L in Boyden's chemotaxis assay (r=0.957,p<0.01). Fibrinogen had no obvious effect on VSMC migration in scrape assay and on VSMC migration at random direction in Time-lapse microcinematography (p>0.05). Fibrinogen induced the up-regulation of expression and activity of glutinase A. Conclusion By recruiting vascular smooth muscle cells from the media into the intima and promoting them proliferate, fibrinogen may be involved in the pathogenesis of atherosclerosis.