OBJECTIVES: To evaluate whether Wnt signalling pathway modulates proliferation and collagen secretion of vascular smooth muscle cells and try to find novel gene target of anti-vascular restenosis. METHODS: Cultured vascular smooth muscle cells (SMC, A7r5) were devided into seven groups: control group; AngII (10 mol/L) group; AngII + atrovastatin (0.1 umol/L) group; AngII + atrovastatin (1 umol/L)group; AngII + atrovastatin (10 umol/L) group; AngII (10mol/L) + SiRNA-dvl-1group; AngII (10mol/L) + SiRNA-dvl-1 + atrovastatin (10 umol/L) group. The SMCs proliferation was determined by MTT assay. Several Wnt genes and proteins werequantitated separatedly by Real-Time quantitative-PCR and Western blot assay. RESULTS: (1) After Dvl-1 Gene was silenced by SiRNA after transcription, proliferation of VSMC induced by AngII was inhibited significantly (AngII + siRNA vs AngII, 0.369 ± 0.105 vs 0.417 ± 0.098, 24h, P < 0.05); Proliferation of VSMC induced by AngII were inhibited significantly by 1umol/L concentrations of atorvastatin in comparison with the control group (0.365 ± 0.077 vs 0.417 ± 0.098, 24h, P < 0.05; 0.321 ± 0.083vs0.434 ± 0.101, 48h, P < 0.05 ; 0.277 ± 0.062 vs 0.425 ± 0.112,72h, P < 0.01), the inhibited effect showed time and concentration dependent manners; (2) High expression of Wnt4, Dvl-1 and ß-catenin mRNA and proteins were induced by AngII, which could be inhibited by atrovastatin in concentration dependent manner (1,10 umol/L vs 0.1 umol/L seperatly, 24 h,wnt4 mRNA:1.188 ± 0.132,0.785 ± 0.246 vs 1.565 ± 0.187, P < 0.05; wnt4 western: 22.73 ± 4.14,15.94 ± 3.38 vs 24.02 ± 5.44, P < 0.05; dvl-1 mRNA:1.254 ± 0.163,1.104 ± 0.086 vs 1.624 ± 0.213, P < 0.05; dvl-1 western: 25.28 ± 4.67,17.57 ± 2.92 vs 27.72 ± 4.29, P < 0.05; ß-catenin mRNA:1.190 ± 0.112,0.986 ± 0.078 vs 1.669 ± 0.194, P < 0.05; ß-catenin western:15.80 ± 3.07,13.67 ± 2.16 vs 28.82 ± 5.10, P < 0.05) and the latter two could be reversed significantly by siRNA-Dvl-1; (3) High expression of collegan I, collegan III mRNA and proteins in VSMC induced by AngII could be inhibited siganificantly by siRNA-Dvl-1 and atrovastatin (1,10 umol/L) (AngII + atv1.0, AngII + atv10 vs AngII, seprately; col1 mRNA 1.660 ± 0.150,1.148 ± 0.091 vs 2.390 ± 0.207, P < 0.05; col1 western 14.02 ± 3.35 vs 16.53 ± 3.86, P > 0.05; 10.12 ± 2.04 vs 16.53 ± 3.86, P < 0.01; col3 mRNA:1.148 ± 0.151, 0.846 ± 0.140 vs 1.552 ± 0.256, P < 0.05; col3 western: 10.23 ± 2.02, 6.35 ± 1.08 vs 18.83 ± 3.45, p < 0.01); (4) After Dvl-1 Gene was silenced by SiRNA, proliferation and collagen secretion of VSMC could be further inhibited by atorvastastin (24 h, AngII + siRNA + atv10 vs AngII + siRNA, MTT: 0.333 ± 0.085 vs 0.369 ± 0.105,p < 0.05; western:col1, 5.86 ± 1.26 vs 8.08 ± 1.88, p < 0.05; col3, 4.18 ± 0.93 vs 6.96 ± 1.14 p < 0.05). CONCLUSIONS: 1) Induced by AngII, VSMC proliferate accompanying with Wnt signal moleculars highly expressed; 2) Expression of intracellular wnt signal moleculars reduced significantly when AngII-induced proliferation of VSMC was inhibited by siRNA-Dvl-1 and atrovastatin; 3) Activation of Wnt signal pathway is involved in AngII-induced high expression of collegan genes in VSMC.4)Wnt signal pathway is involved in AngII-induced VSMC proliferation; 4) Besides wnt signal pathway, any other signal pathways enrolled in AngII-induced VSMC proliferation and collagen secretion.