GW24-e0507 Role of wnt signal pathway in proliferation and collagen secretion of smooth muscle cells from rats aorta induced by AngII

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 -6 mol/L) group; AngII + atrovastatin (0.1 umol/L) group; AngII + atrovastatin (1 umol/L)group; AngII + atrovastatin (10 umol/L) group; AngII (10 -6 mol/L) + SiRNA-dvl-1group; AngII (10 -6 mol/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; 10.12 ± 2.04 vs 16.53 ± 3.86, P 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.