Objective The purpose of this study is to explore the impact of stromal interaction molecule 1 (STIM1) knockdown on the proliferation and migration capacities of endothelial progenitor cells (EPCs).Methods The rat bone marrow derived EPCs were obtained and divided into three groups:adenovirus negative control (NSC) group,rat STIM1 adenovirus vector transfection (si/rSTIM1) group and rat and human recombinant STIM1 adenovirus transfection (si/rSTIM1 + hSTIM1) group.The STIM1 expressions in each group were detected by reverse transcription PCR after transfection.The cell proliferation was tested by [3H] thymidine incorporation assay (3 H-TdR).Cell cycle was analyzed by flow cytometry.The cells migration activity was detected by Boyden assay.Calcium ion concentration was detected by confocal laser scanning microscopy.Results 48 h after transfection,the expression level of STIM1 in si/rSTIM1 group was significantly lower than that in NSC group (0.21 ±0.12 vs.1.01 ±0.01,P ＜0.05),and number of EPCs at G1 phase in si/rSTIM1 group ((93.31 ± 0.24)％) was significantly higher than that in NSC group ((78.03 ± 0.34)％,P ＜ 0.05),and EPCs' migration activity in si/rSTIM1 group (10.03 ± 0.33) was significantly lower than that in NSC group (32.11 ± 0.54,P ＜ 0.05),and EPCs calcium ion concentration in EPCs in si/rSTIM1 group (38.03 ±0.13) was significantly lower than that in NSC group (98.11 ±0.34,P ＜ 0.05),while there was no significant difference between si/rSTIM1 + hSTIM1 group and NSC group on the above four indexes.Conclusion Silencing STIM1 could attenuate EPCs proliferation and migration capacities by modulating the calcium ion concentration in EPCs.