Vitamin C attenuates ERK signalling to inhibit the regulation of collagen production by LL-37 in human dermal fibroblasts

Hyun Jeong Park, Sun Myeong Ock, Hee Jung Kim, Hong Jin Park, Young Bok Lee, Jung Min Choi, Chul Soo Cho, Jun Young Lee, Baik Kee Cho, Dae Ho Cho

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35 Citations (Scopus)


Vitamin C is used as an anti-ageing agent because of its collagen enhancing effects. The precise cellular signalling mechanism of vitamin C is not well known. Here, we investigate the profibrotic mechanism of vitamin C against LL-37. Antimicrobial peptide LL-37 decreases collagen expression at mRNA and protein levels in human dermal fibroblasts (HDFs). The ability of LL-37 to inhibit collagen expression is dependent on phosphorylation of extracellular signal-regulated kinase (ERK). HDFs and human keloid fibroblasts were treated with vitamin C followed by 2 h of LL-37 treatment. Collagen mRNA expression and total soluble collagen production inhibited by LL-37 was enhanced by treatment with 0.5 m. m vitamin C. Vitamin C also decreased intracellular reactive oxygen intermediates (ROI) levels that were increased by LL-37. Furthermore, the phosphorylation of ERK was analysed by Western blot following treatment with vitamin C and LL-37. Vitamin C turned off phosphorylation of ERK that was induced by LL-37. Ets-1 transcriptional factor, which is involved in the regulation of collagen expression by LL-37, was also inhibited by vitamin C. This study shows that vitamin C enhances collagen production by inhibiting the ERK pathway induced by LL-37.

Original languageEnglish
Pages (from-to)e258-e264
JournalExperimental Dermatology
Issue number8
Publication statusPublished - 2010 Aug
Externally publishedYes


  • ERK
  • Human dermal fibroblasts
  • LL-37
  • Vitamin C

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology


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