The gene expression profile of matrix metalloproteinases and their inhibitors in children with Henoch-Schönlein purpura

J. I. Shin, K. S. Song, H. Kim, N. H. Cho, J. Kim, H. S. Kim, J. S. Lee

Research output: Contribution to journalArticle

9 Citations (Scopus)

Abstract

Background Because inflammatory cytokines are known to be potent inducers of matrix metalloproteinases (MMPs), and MMPs themselves can promote inflammation, we speculated that MMP activation might be involved in the pathogenesis of Henoch-Schönlein purpura (HSP) vasculitis. Objectives To investigate the gene expression profile of all known MMPs and tissue inhibitors of metalloproteinases (TIMPs) in children with HSP and to examine the role, if any, of MMPs in the pathogenesis of HSP. Methods Peripheral blood samples were obtained from 10 patients with HSP (nine were in the acute stage, one had HSP nephritis) and four healthy controls. Peripheral blood samples were also taken from the nine patients with HSP when they reached the convalescent stage of the disease. From these samples, total RNA was purified and gene expressions were measured using real-time polymerase chain reaction. Results MMP-8 expression was decreased in patients with arthralgia (P = 0·038), and MMP-3 (P = 0·03) and TIMP-4 expressions (P = 0·016) were elevated in HSP patients with nephritis. Soft tissue oedema was associated with decreased expressions of MMP-26 (P = 0·038) and MMP-28 (P = 0·038). MMP-1, MMP-8, MMP-9, MMP-10, MMP-13, MMP-16 and MMP-26 levels were significantly higher in patients in the acute stage of HSP than in normal controls (P < 0·05). MMP-9 (P = 0·097) and MMP-19 (P = 0·054) levels decreased to borderline significance in patients in the convalescent stage compared with those in the acute stage. The duration of steroid administration was negatively correlated with MMP-1, MMP-2, MMP-7, MMP-10, MMP-12, MMP-19, MMP-23 and TIMP-1 levels (P < 0·05), suggesting a suppressive effect of steroids on the expressions of MMPs and TIMPs. Conclusions This is the first study to describe the expression profile of all known MMPs and TIMPs in children with HSP, and our results suggested that abnormal levels of MMP and TIMP activity may have a role in the pathogenesis of HSP.

Original languageEnglish
Pages (from-to)1348-1355
Number of pages8
JournalBritish Journal of Dermatology
Volume164
Issue number6
DOIs
Publication statusPublished - 2011 Jun 1

Fingerprint

Schoenlein-Henoch Purpura
Matrix Metalloproteinase Inhibitors
Transcriptome
Matrix Metalloproteinases
Tissue Inhibitor of Metalloproteinases
Matrix Metalloproteinase 10
Matrix Metalloproteinase 8
Matrix Metalloproteinase 1
Nephritis
Matrix Metalloproteinase 9
Matrix Metalloproteinase 16
Matrix Metalloproteinase 12
Steroids
Matrix Metalloproteinase 7
Matrix Metalloproteinase 13
Matrix Metalloproteinase 3
Tissue Inhibitor of Metalloproteinase-1
Matrix Metalloproteinase 2
Arthralgia
Vasculitis

All Science Journal Classification (ASJC) codes

  • Dermatology

Cite this

@article{bec1d5eda5d544819b208e73d2650a03,
title = "The gene expression profile of matrix metalloproteinases and their inhibitors in children with Henoch-Sch{\"o}nlein purpura",
abstract = "Background Because inflammatory cytokines are known to be potent inducers of matrix metalloproteinases (MMPs), and MMPs themselves can promote inflammation, we speculated that MMP activation might be involved in the pathogenesis of Henoch-Sch{\"o}nlein purpura (HSP) vasculitis. Objectives To investigate the gene expression profile of all known MMPs and tissue inhibitors of metalloproteinases (TIMPs) in children with HSP and to examine the role, if any, of MMPs in the pathogenesis of HSP. Methods Peripheral blood samples were obtained from 10 patients with HSP (nine were in the acute stage, one had HSP nephritis) and four healthy controls. Peripheral blood samples were also taken from the nine patients with HSP when they reached the convalescent stage of the disease. From these samples, total RNA was purified and gene expressions were measured using real-time polymerase chain reaction. Results MMP-8 expression was decreased in patients with arthralgia (P = 0·038), and MMP-3 (P = 0·03) and TIMP-4 expressions (P = 0·016) were elevated in HSP patients with nephritis. Soft tissue oedema was associated with decreased expressions of MMP-26 (P = 0·038) and MMP-28 (P = 0·038). MMP-1, MMP-8, MMP-9, MMP-10, MMP-13, MMP-16 and MMP-26 levels were significantly higher in patients in the acute stage of HSP than in normal controls (P < 0·05). MMP-9 (P = 0·097) and MMP-19 (P = 0·054) levels decreased to borderline significance in patients in the convalescent stage compared with those in the acute stage. The duration of steroid administration was negatively correlated with MMP-1, MMP-2, MMP-7, MMP-10, MMP-12, MMP-19, MMP-23 and TIMP-1 levels (P < 0·05), suggesting a suppressive effect of steroids on the expressions of MMPs and TIMPs. Conclusions This is the first study to describe the expression profile of all known MMPs and TIMPs in children with HSP, and our results suggested that abnormal levels of MMP and TIMP activity may have a role in the pathogenesis of HSP.",
author = "Shin, {J. I.} and Song, {K. S.} and H. Kim and Cho, {N. H.} and J. Kim and Kim, {H. S.} and Lee, {J. S.}",
year = "2011",
month = "6",
day = "1",
doi = "10.1111/j.1365-2133.2011.10295.x",
language = "English",
volume = "164",
pages = "1348--1355",
journal = "British Journal of Dermatology",
issn = "0007-0963",
publisher = "Wiley-Blackwell",
number = "6",

}

The gene expression profile of matrix metalloproteinases and their inhibitors in children with Henoch-Schönlein purpura. / Shin, J. I.; Song, K. S.; Kim, H.; Cho, N. H.; Kim, J.; Kim, H. S.; Lee, J. S.

In: British Journal of Dermatology, Vol. 164, No. 6, 01.06.2011, p. 1348-1355.

Research output: Contribution to journalArticle

TY - JOUR

T1 - The gene expression profile of matrix metalloproteinases and their inhibitors in children with Henoch-Schönlein purpura

AU - Shin, J. I.

AU - Song, K. S.

AU - Kim, H.

AU - Cho, N. H.

AU - Kim, J.

AU - Kim, H. S.

AU - Lee, J. S.

PY - 2011/6/1

Y1 - 2011/6/1

N2 - Background Because inflammatory cytokines are known to be potent inducers of matrix metalloproteinases (MMPs), and MMPs themselves can promote inflammation, we speculated that MMP activation might be involved in the pathogenesis of Henoch-Schönlein purpura (HSP) vasculitis. Objectives To investigate the gene expression profile of all known MMPs and tissue inhibitors of metalloproteinases (TIMPs) in children with HSP and to examine the role, if any, of MMPs in the pathogenesis of HSP. Methods Peripheral blood samples were obtained from 10 patients with HSP (nine were in the acute stage, one had HSP nephritis) and four healthy controls. Peripheral blood samples were also taken from the nine patients with HSP when they reached the convalescent stage of the disease. From these samples, total RNA was purified and gene expressions were measured using real-time polymerase chain reaction. Results MMP-8 expression was decreased in patients with arthralgia (P = 0·038), and MMP-3 (P = 0·03) and TIMP-4 expressions (P = 0·016) were elevated in HSP patients with nephritis. Soft tissue oedema was associated with decreased expressions of MMP-26 (P = 0·038) and MMP-28 (P = 0·038). MMP-1, MMP-8, MMP-9, MMP-10, MMP-13, MMP-16 and MMP-26 levels were significantly higher in patients in the acute stage of HSP than in normal controls (P < 0·05). MMP-9 (P = 0·097) and MMP-19 (P = 0·054) levels decreased to borderline significance in patients in the convalescent stage compared with those in the acute stage. The duration of steroid administration was negatively correlated with MMP-1, MMP-2, MMP-7, MMP-10, MMP-12, MMP-19, MMP-23 and TIMP-1 levels (P < 0·05), suggesting a suppressive effect of steroids on the expressions of MMPs and TIMPs. Conclusions This is the first study to describe the expression profile of all known MMPs and TIMPs in children with HSP, and our results suggested that abnormal levels of MMP and TIMP activity may have a role in the pathogenesis of HSP.

AB - Background Because inflammatory cytokines are known to be potent inducers of matrix metalloproteinases (MMPs), and MMPs themselves can promote inflammation, we speculated that MMP activation might be involved in the pathogenesis of Henoch-Schönlein purpura (HSP) vasculitis. Objectives To investigate the gene expression profile of all known MMPs and tissue inhibitors of metalloproteinases (TIMPs) in children with HSP and to examine the role, if any, of MMPs in the pathogenesis of HSP. Methods Peripheral blood samples were obtained from 10 patients with HSP (nine were in the acute stage, one had HSP nephritis) and four healthy controls. Peripheral blood samples were also taken from the nine patients with HSP when they reached the convalescent stage of the disease. From these samples, total RNA was purified and gene expressions were measured using real-time polymerase chain reaction. Results MMP-8 expression was decreased in patients with arthralgia (P = 0·038), and MMP-3 (P = 0·03) and TIMP-4 expressions (P = 0·016) were elevated in HSP patients with nephritis. Soft tissue oedema was associated with decreased expressions of MMP-26 (P = 0·038) and MMP-28 (P = 0·038). MMP-1, MMP-8, MMP-9, MMP-10, MMP-13, MMP-16 and MMP-26 levels were significantly higher in patients in the acute stage of HSP than in normal controls (P < 0·05). MMP-9 (P = 0·097) and MMP-19 (P = 0·054) levels decreased to borderline significance in patients in the convalescent stage compared with those in the acute stage. The duration of steroid administration was negatively correlated with MMP-1, MMP-2, MMP-7, MMP-10, MMP-12, MMP-19, MMP-23 and TIMP-1 levels (P < 0·05), suggesting a suppressive effect of steroids on the expressions of MMPs and TIMPs. Conclusions This is the first study to describe the expression profile of all known MMPs and TIMPs in children with HSP, and our results suggested that abnormal levels of MMP and TIMP activity may have a role in the pathogenesis of HSP.

UR - http://www.scopus.com/inward/record.url?scp=79957600358&partnerID=8YFLogxK

UR - http://www.scopus.com/inward/citedby.url?scp=79957600358&partnerID=8YFLogxK

U2 - 10.1111/j.1365-2133.2011.10295.x

DO - 10.1111/j.1365-2133.2011.10295.x

M3 - Article

C2 - 21410660

AN - SCOPUS:79957600358

VL - 164

SP - 1348

EP - 1355

JO - British Journal of Dermatology

JF - British Journal of Dermatology

SN - 0007-0963

IS - 6

ER -