PMID- 23815460
OWN - NLM
STAT- MEDLINE
DCOM- 20150918
LR  - 20140211
IS  - 1365-2591 (Electronic)
IS  - 0143-2885 (Linking)
VI  - 47
IP  - 3
DP  - 2014 Mar
TI  - Involvement of SDF-1 and monocyte chemoattractant protein-1 in hydrogen 
      peroxide-induced extracellular matrix degradation in human dental pulp cells.
PG  - 298-308
LID - 10.1111/iej.12147 [doi]
AB  - AIM: To determine whether chemokines such as SDF-1 and monocyte chemoattractant 
      protein-1 (MCP-1) are responsible for hydrogen peroxide (H2 O2 )-induced 
      extracellular matrix (ECM) degradation and to identify the underlying mechanism 
      in human dental pulp cells (HDPCs). METHOD: Human dental pulp cells were exposed 
      to 0.4 mmol H2 O2 for 48 h. mRNA expression and protein expression were examined 
      by RT-PCR and Western blot analysis, respectively. The mRNA expression of 
      chemokine (SDF-1 and MCP-1), their receptors (CXCR4 and CXCR2) and extracellular 
      matrix proteins was evaluated by reverse transcriptase-polymerase chain reaction. 
      The production of SDF-1, MCP-1, CXCR4 and CCR2 in the culture medium was 
      determined by enzyme-linked immunosorbent assay. Signal transduction pathway was 
      examined by Western blotting. RESULTS: Hydrogen peroxide provoked the activation 
      of MCP-1 and SDF-1 mRNA and their respective receptors, CXCR4 and CXCR2. H2 O2 
      treatment concomitantly downregulated the expression of ECM molecules, such as 
      type I collagen, elastin and fibronectin, and upregulated the mRNA expression of 
      matrix metalloproteinase-1 (MMP-1), MMP-2, MMP-8 and MMP-9. Hydrogen 
      peroxide-induced ECM degradation and MMP upregulation were blocked by 
      neutralizing antibodies and siRNAs directed against SDF-1 and MCP-1. Inhibition 
      of SDF-1 and MCP-1 blocked the H2 O2 -induced activation of Akt, p38, ERK and 
      NF-kB. CONCLUSION: Inhibition of SDF and MCP-1 is a potent component of reducing 
      release reactive oxygen species-induced ECM degradation in HDPCs and may play an 
      important role in pulpal and periapical inflammation.
CI  - (c) 2013 International Endodontic Journal. Published by John Wiley & Sons Ltd.
FAU - Kim, D-S
AU  - Kim DS
AD  - Department of Conservative Dentistry, School of Dentistry and Institute of Oral 
      Biology, Kyung Hee University, Seoul, Korea.
FAU - Kang, S I
AU  - Kang SI
FAU - Lee, S-Y
AU  - Lee SY
FAU - Noh, K-T
AU  - Noh KT
FAU - Kim, E-C
AU  - Kim EC
LA  - eng
PT  - Journal Article
PT  - Research Support, Non-U.S. Gov't
DEP - 20130701
PL  - England
TA  - Int Endod J
JT  - International endodontic journal
JID - 8004996
RN  - 0 (CXCL12 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Chemokine CXCL12)
RN  - 0 (RNA, Messenger)
RN  - 0 (Reactive Oxygen Species)
RN  - BBX060AN9V (Hydrogen Peroxide)
RN  - EC 3.4.24.- (Matrix Metalloproteinases)
MH  - Blotting, Western
MH  - Cells, Cultured
MH  - Chemokine CCL2/*metabolism
MH  - Chemokine CXCL12/*metabolism
MH  - Dental Pulp/*cytology
MH  - Enzyme-Linked Immunosorbent Assay
MH  - Extracellular Matrix/*drug effects/*metabolism
MH  - Humans
MH  - Hydrogen Peroxide/*pharmacology
MH  - Matrix Metalloproteinases/metabolism
MH  - RNA, Messenger/metabolism
MH  - Reactive Oxygen Species/metabolism
MH  - Reverse Transcriptase Polymerase Chain Reaction
MH  - Signal Transduction
OTO - NOTNLM
OT  - SDF-1
OT  - extracellular matrix
OT  - human dental pulp cells
OT  - hydrogen peroxide
OT  - matrix metalloprotein
OT  - monocyte chemoattractant protein-1
EDAT- 2013/07/03 06:00
MHDA- 2015/09/19 06:00
CRDT- 2013/07/03 06:00
PHST- 2012/11/28 00:00 [received]
PHST- 2013/06/03 00:00 [accepted]
PHST- 2013/07/03 06:00 [entrez]
PHST- 2013/07/03 06:00 [pubmed]
PHST- 2015/09/19 06:00 [medline]
AID - 10.1111/iej.12147 [doi]
PST - ppublish
SO  - Int Endod J. 2014 Mar;47(3):298-308. doi: 10.1111/iej.12147. Epub 2013 Jul 1.