Premium
LL‐37 suppresses sodium nitroprusside‐induced apoptosis of systemic sclerosis dermal fibroblasts
Author(s) -
Kim Hee Jung,
Cho Dae Ho,
Lee Kyung Jin,
Cho Chul Soo,
Bang Sa Ik,
Cho Baik Kee,
Park Hyun Jeong
Publication year - 2011
Publication title -
experimental dermatology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.108
H-Index - 96
eISSN - 1600-0625
pISSN - 0906-6705
DOI - 10.1111/j.1600-0625.2011.01327.x
Subject(s) - apoptosis , sodium nitroprusside , mapk/erk pathway , fibroblast , cathelicidin , chemistry , microbiology and biotechnology , cancer research , signal transduction , endocrinology , biology , antimicrobial peptides , peptide , nitric oxide , biochemistry , in vitro
Abstract: 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.