Silence of STIM1 attenua=tes the proliferation and migration of EPCs after vascular injury and its mechanism

Abstract

ObjectiveTo 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. MethodsThe 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 [3H] thymidine incorporation assay (3H-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. Results48 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. ConclusionsSilence of STIM1 attenuates EPCs proliferation and migration after vascular injury, by mediating the calcium ion concentration in EPCs.