Journal
EXPERIMENTAL DERMATOLOGY
Volume 28, Issue 1, Pages 19-27Publisher
WILEY
DOI: 10.1111/exd.13800
Keywords
Dpp4; high glucose; hypertrophic scar-derived fibroblasts; IGF/Akt/mTOR signalling pathway; linagliptin
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Hypertrophic scar (HS) is a fibroproliferative disease after serious burns; the underlying mechanism remains unknown. The study was performed to clarify the effect of high glucose (HG) on HS. The expression of Col1, Col3 and alpha-SMA was upregulated in HS-derived fibroblasts (HSF) exposed to HG (20 and 30 mmol/L), and HG activated the phosphorylated protein expression of IGF/Akt/mTOR signalling pathway in HSF. Dpp4, a marker targeted the treatment of diabetes mellitus, was overexpressed in HG-induced HSF. Linagliptin, a Dpp4 inhibitor, played the antifibrotic role in HSF exposed to HG, the levels of Col1, Col3 and alpha-SMA were significantly downregulated, and the cell proliferation and migration were also inhibited. Furthermore, linagliptin alleviated the phosphorylated protein expression of IGF/Akt/mTOR signalling pathway. Moreover, the mTOR inhibitor (rapamycin) mimicked the effect of linagliptin on the collagen and alpha-SMA that means linagliptin may inhibit HG-induced transdifferentiation of HSF to myofibroblasts via IGF/Akt/mTOR signalling pathway.
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