Silence of STIM1 attenuates the proliferation and migration of EPCs after vascular injury and its mechanism.

Objective: To investigate the effect of stromal interaction molecule 1(STIM1) knockdown on the proliferation and migration of endothelial progenitor cells (EPCs) after vascular injury and its mechanism.

Methods: The rat bone marrow derived EPCs were divided into three groups: adenovirus negative control (group NSC), rat STIM1 adenovirus vector transfection group (group si/rSTIM1) and rat &human recombinant STIM1 adenovirus transfection group (group si/rSTIM1+hSTIM1). The STIM1 expressions in each group were detected by reverse transcription PCR after transfection; the cell proliferation was tested by [(3)H] 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 using laser confocal method.

Results: 48 h later after transfection, the expression level of STIM1 in si/rSTIM1 cells was significantly lower than that in NSC group (0.21 ± 0.12 vs 1.01 ± 0.01, P<0.05); EPCs that stayed in G1 phase in si/rSTIM1 group [(93.31 ± 0.24)%] were significantly more than that in NSC group [(78.03 ± 0.34)%, P<0.05]; 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); EPCs calcium ion concentration changes 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 four indexes above.

Conclusions: Silence of STIM1 attenuates EPCs proliferation and migration after vascular injury, by mediating the calcium ion concentration in EPCs.