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 journalLetter

18 Citations (Scopus)

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.

Original languageEnglish
Pages (from-to)843-845
Number of pages3
JournalExperimental Dermatology
Volume20
Issue number10
DOIs
Publication statusPublished - 2011 Oct 1
Externally publishedYes

Fingerprint

Systemic Scleroderma
Nitroprusside
Fibroblasts
Apoptosis
Skin
Phosphorylation
Sclerosis
Prostaglandins E
Caspase 3
Chemical activation
Immunohistochemistry
Proteins

Keywords

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

ASJC Scopus subject areas

  • Biochemistry
  • Molecular Biology
  • Dermatology

Cite this

LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts. / Kim, Hee Jung; Cho, Dae Ho; Lee, Kyung Jin; Cho, Chul Soo; Bang, Sa Ik; Cho, Baik Kee; Park, Hyun Jeong.

In: Experimental Dermatology, Vol. 20, No. 10, 01.10.2011, p. 843-845.

Research output: Contribution to journalLetter

Kim, Hee Jung ; Cho, Dae Ho ; Lee, Kyung Jin ; Cho, Chul Soo ; Bang, Sa Ik ; Cho, Baik Kee ; Park, Hyun Jeong. / LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts. In: Experimental Dermatology. 2011 ; Vol. 20, No. 10. pp. 843-845.
@article{3555ed42e1c64daf8a44e39877166f9a,
title = "LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts",
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.",
keywords = "Antimicrobial peptide, Apoptosis, Human dermal fibroblasts, LL-37, Systemic sclerosis",
author = "Kim, {Hee Jung} and Cho, {Dae Ho} and Lee, {Kyung Jin} and Cho, {Chul Soo} and Bang, {Sa Ik} and Cho, {Baik Kee} and Park, {Hyun Jeong}",
year = "2011",
month = "10",
day = "1",
doi = "10.1111/j.1600-0625.2011.01327.x",
language = "English",
volume = "20",
pages = "843--845",
journal = "Experimental Dermatology",
issn = "0906-6705",
publisher = "Wiley-Blackwell",
number = "10",

}

TY - JOUR

T1 - LL-37 suppresses sodium nitroprusside-induced apoptosis of systemic sclerosis dermal fibroblasts

AU - Kim, Hee Jung

AU - Cho, Dae Ho

AU - Lee, Kyung Jin

AU - Cho, Chul Soo

AU - Bang, Sa Ik

AU - Cho, Baik Kee

AU - Park, Hyun Jeong

PY - 2011/10/1

Y1 - 2011/10/1

N2 - 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.

AB - 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.

KW - Antimicrobial peptide

KW - Apoptosis

KW - Human dermal fibroblasts

KW - LL-37

KW - Systemic sclerosis

UR - http://www.scopus.com/inward/record.url?scp=80052968673&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=80052968673&partnerID=8YFLogxK

U2 - 10.1111/j.1600-0625.2011.01327.x

DO - 10.1111/j.1600-0625.2011.01327.x

M3 - Letter

C2 - 21732986

AN - SCOPUS:80052968673

VL - 20

SP - 843

EP - 845

JO - Experimental Dermatology

JF - Experimental Dermatology

SN - 0906-6705

IS - 10

ER -