LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts

Hee Jung Kim, Dae Ho Cho, Kyung Jin Lee, Chul Soo Cho, Sa Ik Bang, Baik Kee Cho, Hyun Jeong Park

Research output: Contribution to journalLetterpeer-review

26 Citations (Scopus)


The human cathelicidin antimicrobial peptide LL-37 regulates apoptosis of several cell types. Defective apoptosis of skin fibroblasts may contribute to systemic sclerosis (SSc). Here, we show that LL-37 inhibited apoptosis of SSc fibroblasts and identified the signalling pathways by which LL-37 mediates apoptosis. Immunohistochemistry showed that cathelicidin expression was enhanced in SSc patients compared with healthy controls. In addition, LL-37 decreased sodium nitroprusside (SNP)-induced apoptosis of SSc fibroblasts. LL-37 significantly increased expression of Bcl-2 and decreased levels of BAX protein. Pretreatment with LL-37 decreased activation of caspase-3 following SNP-treatment. Moreover, exposure of SSc fibroblasts to LL-37 resulted in increased expression of COX-2 and stimulation of prostaglandin E 2 (PGE 2). Furthermore, LL-37 induced phosphorylation of ERK and the ERK inhibitor PD98059 blocked the inhibitory effect of LL-37 on apoptosis. Our data indicate that LL-37 may be associated with skin sclerosis by inhibiting apoptosis of dermal fibroblasts.

Original languageEnglish
Pages (from-to)843-845
Number of pages3
JournalExperimental Dermatology
Issue number10
Publication statusPublished - 2011 Oct
Externally publishedYes


  • Antimicrobial peptide
  • Apoptosis
  • Human dermal fibroblasts
  • LL-37
  • Systemic sclerosis

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology


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