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VEGF165 attenuates the Th17/Treg imbalance that exists when transplanting allogeneic skeletal myoblasts to treat acute myocardial infarction

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Abstract

Objectives

To investigate whether Th17/Treg imbalance exists, and whether VEGF165 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 VEGF165 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 VEGF165 was able to relieve the severity of the Th17/Treg imbalance.

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Acknowledgments

We are grateful for the support of Natural Science Foundation of Shanghai (Grant No. 10ZR1406200100), and the National Natural Science Foundation of China (Grant No. 81000042).

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Correspondence to Ruijun Liu, Changfa Guo or Chunsheng Wang.

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Responsible Editor: Liwu Li.

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Liu, R., Guo, C., Yang, C. et al. VEGF165 attenuates the Th17/Treg imbalance that exists when transplanting allogeneic skeletal myoblasts to treat acute myocardial infarction. Inflamm. Res. 62, 69–79 (2013). https://doi.org/10.1007/s00011-012-0553-4

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  • DOI: https://doi.org/10.1007/s00011-012-0553-4

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