Ｏbjective： To investigate the effect of miR-155 on cell cycle progression of mice vascular smooth muscle cells under treatment of AngⅡ， and explore the detailed mechanism. Methods： The vascular smooth muscle cells（VSMCs） derived from C57 mice were cultured by the adherent method （1×10-6 mol/L AngⅡ for 48 h）. Quantitative real-time PCR （q-RT-PCR） was performed to detect the miR-155 expression levels of the blank control group and the Ang Ⅱ group. q-RT-PCR and Western blot assay were performed to detect the mRNA and protein levels of angiotensin Ⅱ type 1 receptor（AT1R） in the transfected miR-155 group and the negative control group; Western blot assay was performed to detect the effect of transfected miR-155 mimics and negative control group on extracellular signal-regulated kinase 1/2 （ERK1/2） of AT1R downstream and ribosomal protein S6 kinase （P70S6K1） signaling pathway. The expression of cyclin D1（Cyclin D1） was examined by transfection of miR-155 mimics，angiotensin receptor blocker valsartan，mTOR pathway inhibitor rapamycin，and ERK1/2 inhibitor U0126. In the end，we used flow cytometer to analyze the change of cell cycle to investigate the effect of miR-155 on cell cycle and its mechanism. Results： AngⅡ significantly decreased the expression of miR-155. miR-155 mimics remarkably attenuated AT1R expression from mRNA and protein levels，inhibited the AngⅡ-activated ERK1/2 and P70S6K signaling pathway，and decreased the AngⅡ-enforced expression of Cyclin D1. Transfection of miR-155，valsartan，rapamycin and U0126 suppressed the AngⅡ-induced G1-to S-phase progression of VSMC. Conclusion： MiR-155 can inhibit the expression of AngⅡ-induced ERK1/2，activation of P70S6K1 signaling pathway，and Cyclin D1 by blocking AT1R，and thereby inhibit the function of Ang Ⅱ-induced cell cycle transition.