title: [Stromal interaction molecule 1 silencing attenuates the proliferation and migration capacities of endothelial progenitor cells].
abstract: 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 [(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 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.
  
  
  CONCLUSIONS
  Silencing STIM1 could attenuate EPCs proliferation and migration capacities by modulating the calcium ion concentration in EPCs.
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China.
authors.forename: Wenhui
authors.initials: W
authors.lastname: Wang
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China.
authors.forename: Xinming
authors.initials: X
authors.lastname: Li
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China. Email: zpyykjkll@126.com.
authors.forename: Liang
authors.initials: L
authors.lastname: Liu
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China.
authors.forename: Jiayin
authors.initials: J
authors.lastname: Hou
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China.
authors.forename: Qian
authors.initials: Q
authors.lastname: Zhu
authors.affiliation: Department of Cardiology, Shanghai Pudong New Area Zhoupu Hospital, Shanghai 200092, China.
authors.forename: Xinpeng
authors.initials: X
authors.lastname: Cong
mesh_terms: D000256:Adenoviridae; D000818:Animals; D002453:Cell Cycle; D002455:Cell Division; D002465:Cell Movement; D049109:Cell Proliferation; D042783:Endothelial Cells; D066026:Endothelial Progenitor Cells; D005434:Flow Cytometry; D005822:Genetic Vectors; D006801:Humans; D008565:Membrane Proteins; D009363:Neoplasm Proteins; D051381:Rats; D000071737:Stromal Interaction Molecule 1; D014162:Transfection
chemical_list: D008565:Membrane Proteins; D009363:Neoplasm Proteins; C103530:STIM1 protein, human; D000071737:Stromal Interaction Molecule 1