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MicroRNA-152-5p inhibits proliferation and migration and promotes apoptosis by regulating expression of Smad3 in human keloid fibroblasts

  • Pang, Qianqian (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Wang, Yuming (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Xu, Mingyuan (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Xu, Jiachao (Department of Internal Medicine, Haiyan Hospital of Traditional Chinese Medicine) ;
  • Xu, Shengquan (Department of Hand Surgery and Microsurgery Center, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Shen, Yichen (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Xu, Jinghong (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University) ;
  • Lei, Rui (Department of Plastic Surgery, The First Affiliated Hospital, School of Medicine, Zhejiang University)
  • Received : 2018.12.04
  • Accepted : 2019.01.05
  • Published : 2019.03.31

Abstract

Keloids are the most common pathological form of trauma healing, with features that seriously affect appearance and body function, are difficult to treat and have a high recurrence rate. Emerging evidence suggests that miRNAs are involved in a variety of pathological processes and play an important role in the process of fibrosis. In this study, we investigated the function and regulatory network of miR-152-5p in keloids. The miRNA miR-152-5p is frequently downregulated in keloid tissue and primary cells compared to normal skin tissue and fibroblasts. In addition, the downregulation of miR-152-5p is significantly associated with the proliferation, migration and apoptosis of keloid cells. Overexpression of miR-152-5p significantly inhibits the progression of fibrosis in keloids. Smad3 is a direct target of miR-152-5p, and knockdown of Smad3 also inhibits fibrosis progression, consistent with the overexpression of miR-152-5p. The interaction between miR-152-5p and Smad3 occurs through the Erk1/2 and Akt pathways and regulates collagen3 production. In summary, our study demonstrates that miR-152-5p/Smad3 regulatory pathways involved in fibrotic progression may be a potential therapeutic target of keloids.

Keywords

References

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