LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts
- Authors
- Kim, Hee Jung; Cho, Dae Ho; Lee, Kyung Jin; Cho, Chul Soo; Bang, Sa Ik; Cho, Baik Kee; Park, Hyun Jeong
- Issue Date
- Oct-2011
- Publisher
- WILEY-BLACKWELL
- Keywords
- antimicrobial peptide; apoptosis; human dermal fibroblasts; LL-37; systemic sclerosis
- Citation
- EXPERIMENTAL DERMATOLOGY, v.20, no.10, pp 843 - 845
- Pages
- 3
- Journal Title
- EXPERIMENTAL DERMATOLOGY
- Volume
- 20
- Number
- 10
- Start Page
- 843
- End Page
- 845
- URI
- https://scholarworks.sookmyung.ac.kr/handle/2020.sw.sookmyung/12485
- DOI
- 10.1111/j.1600-0625.2011.01327.x
- ISSN
- 0906-6705
1600-0625
- 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.
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