2. Academic Validation
  3. Endogenous peptide LYENRL prevents the activation of hypertrophic scar-derived fibroblasts by inhibiting the TGF-β1/Smad pathway

Endogenous peptide LYENRL prevents the activation of hypertrophic scar-derived fibroblasts by inhibiting the TGF-β1/Smad pathway

  • Life Sci. 2019 Aug 15;231:116674. doi: 10.1016/j.lfs.2019.116674.
Xiaojun Ji 1,  Zhe Tang 2,  Weiwei Shuai 2,  Zhirui Zhang 1,  Jingyun Li 3,  Ling Chen 4,  Jing Cao 5,  Wu Yin 6
Affiliations

Affiliations

  • 1 State Key Lab of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210046, China.
  • 2 Department of Pharmacy, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing 210004, China.
  • 3 Nanjing Maternal and Child Health Medical Institute, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing 210004, China.
  • 4 Department of Plastic & Cosmetic Surgery, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing 210004, China.
  • 5 Department of Pharmacy, Women's Hospital of Nanjing Medical University (Nanjing Maternity and Child Health Care Hospital), Nanjing 210004, China. Electronic address: njfycj@163.com.
  • 6 State Key Lab of Pharmaceutical Biotechnology, College of Life Sciences, Nanjing University, Nanjing 210046, China. Electronic address: wyin@nju.edu.cn.
PMID: 31344427 DOI: 10.1016/j.lfs.2019.116674
Abstract

Hypertrophic scar formation is a fibroproliferative disorder caused by abnormal wound healing. At present, there are limited treatment strategies for hypertrophic scars. In this study, we identified an endogenous peptide, LYENRL, through peptidomics screening that is downregulated in scar skin tissues. The peptide exhibited concentration dependent inhibitory effects on the proliferation, migration and extracellular matrix (ECM) production of scar fibroblasts. By eukaryotic transcriptome sequencing analysis, we noted that LYENRL downregulated gene sets in scar fibroblasts were associated with the Transforming Growth Factor-β (TGF-β) signaling pathway. Further experiments revealed that LYENRL was able to inhibit the activation of TGF-β1/Smad signaling and TGF-β1-induced activation of scar fibroblasts at the source by blocking the binding of AP-1 to the corresponding region of the Tgfb1 promoter, which in turn inhibited gene expression of Tgfb1. Taken together, we concluded that the effects of LYENRL on scar fibroblasts make it a potential peptide drug for hypertrophic scar treatment.

Keywords

Endogenous peptide; Fibroblasts; Hypertrophic scars; LYENRL; TGF-β1/Smad.

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