title: VEGF165 attenuates the Th17/Treg imbalance that exists when transplanting allogeneic skeletal myoblasts to treat acute myocardial infarction.
abstract: OBJECTIVE
  To investigate whether Th17/Treg imbalance exists, and whether VEGF(165) attenuates the imbalance in allogeneic skeletal myoblast transplantation (allo-SMT) for acute myocardial infarction (AMI).
  
  
  METHODS
  On days 1, 2, 4, and 7 after allo-SMT, the percentages and ratios of Th17 and Treg cells were analyzed by flow cytometry in three groups-the AMI group, the AMI-S group (allo-SMT) and the AMI-V group (with VEGF(165) treatment). Subsequently, related proinflammatory and regulatory cytokines and key transcription factors, ROR-γt mRNA and Foxp3 mRNA expression, were examined by Bio-plex and real-time polymerase chain reaction, respectively.
  
  
  RESULTS
  On days 1, 2, 4, and 7, the percentage of Tregs, related cytokine concentrations and transcript factor Foxp3 mRNA in the AMI-S group were lower than those in the AMI group, while those in the AMI-V group were higher than those in the AMI group. However, the percentage of Th17 cells, related cytokine concentrations and ROR-γt mRNA in the AMI-S group were higher than those in the AMI group; those in the AMI-V group were lower than those in the AMI group. Compared with the AMI group, the ratios of Th17/Treg cells significantly increased in the AMI-S group and decreased in the AMI-V group.
  
  
  CONCLUSIONS
  Th17/Treg imbalance participated in the formation and development of the inflammatory and immune response after allo-SMT. However, transfected VEGF(165) was able to relieve the severity of the Th17/Treg imbalance.
authors.affiliation: Department of Cardiac Surgery, Zhongshan Hospital, Fudan University & Shanghai Institute of Cardiovascular Diseases, No. 180 Fenglin Road, Xuhui District, Shanghai, People's Republic of China. iamliuruijun@126.com
authors.forename: Ruijun
authors.initials: R
authors.lastname: Liu
authors.forename: Changfa
authors.initials: C
authors.lastname: Guo
authors.forename: Chen
authors.initials: C
authors.lastname: Yang
authors.forename: Demin
authors.initials: D
authors.lastname: Xu
authors.forename: Chunsheng
authors.initials: C
authors.lastname: Wang
mesh_terms: D000818:Animals; D005455:Fluorescent Antibody Technique; D051858:Forkhead Transcription Factors / Q000235:genetics; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D032448:Myoblasts, Skeletal / Q000637:transplantation*; D009203:Myocardial Infarction / Q000276:immunology / Q000601:surgery*; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3 / Q000235:genetics; D012333:RNA, Messenger / Q000032:analysis; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D058504:Th17 Cells / Q000276:immunology*; D014162:Transfection; D014184:Transplantation, Homologous; D042461:Vascular Endothelial Growth Factor A / Q000502:physiology*
chemical_list: D051858:Forkhead Transcription Factors; C498833:Foxp3 protein, mouse; D057132:Nuclear Receptor Subfamily 1, Group F, Member 3; D012333:RNA, Messenger; D042461:Vascular Endothelial Growth Factor A; C467480:vascular endothelial growth factor A, mouse