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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/rSTlM1+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(~3HTdR);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 G_1 phase in si/rSTIM1 group[(93.3l±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/rSTIM1group(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.
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 STIM1 adenovirus vector transfection group (group si / rSTIM1) and rat & human recombinant STIM1 adenovirus transfection group (group si / rSTlM1 + hSTIM1). The STIM1 expressions in each group were detected by reverse transcription PCR after transfection; Cell cycle was detected by flow cytometry; the cells’ migration activity was detected by Boyden assay; Calcium ion concentration was detected by using laser confocal method. Results: The cell proliferation was detected by [~ 3H] thymidine incorporation assay 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 G_1 (93.31 ± 0.24)%] were significantly more than those 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 / rSTIM1group (38.03 ± 0.13) 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.