PMID- 16244112
OWN - NLM
STAT- MEDLINE
DCOM- 20060302
LR  - 20181203
IS  - 0741-5400 (Print)
IS  - 0741-5400 (Linking)
VI  - 79
IP  - 1
DP  - 2006 Jan
TI  - Synergistic enhancement of cytokine-induced human monocyte matrix 
      metalloproteinase-1 by C-reactive protein and oxidized LDL through differential 
      regulation of monocyte chemotactic protein-1 and prostaglandin E2.
PG  - 105-13
AB  - C-reactive protein (CRP) and oxidized LDL (ox-LDL) are associated with 
      inflammatory lesions, such as coronary artery disease, in which monocytes and 
      matrix metalloproteinases (MMPs) may play a major role in the rupture of 
      atherosclerotic plaques. Monocytes are recruited to inflammation sites by 
      monocyte chemoattractant protein-1 (MCP-1), which may also participate in the 
      activation of monocytes. The objective of this study was to compare the 
      individual and combined effect of CRP and ox-LDL on human monocyte MMP-1 and the 
      role of MCP-1 in this effect. Although CRP or ox-LDL failed to induce MMP-1 in 
      control monocytes, these molecules enhanced MMP-1 production induced by tumor 
      necrosis factor alpha (TNF-alpha) and granulocyte macrophage-colony stimulating 
      factor (GM-CSF) with a synergistic increase in MMP-1 occurring in the presence of 
      both mediators. Enhancement of MMP-1 by CRP and ox-LDL was attributable to a 
      differential increase in MCP-1 and prostaglandin E2(PGE2). CRP, at physiological 
      concentrations, induced high levels of MCP-1 and relatively low levels of PGE2, 
      whereas ox-LDL caused a significant enhancement of PGE2 with little affect on 
      MCP-1. Accordingly, CRP- and ox-LDL-induced MMP-1 production by monocytes was 
      inhibited by anti-MCP-1 antibodies and indomethacin, respectively. Moreover, 
      addition of exogenous MCP-1 or PGE2 enhanced MMP-1 production by TNF-alpha- and 
      GM-CSF-stimulated monocytes. These results show that the combination of CRP and 
      ox-LDL can cause a synergistic enhancement of the role of monocytes in 
      inflammation, first, by increasing MCP-1, which attracts more monocytes and 
      directly enhances MMP-1 production by activated monocytes, and second, by 
      elevating PGE2 production, which also leads to higher levels of MMP-1.
FAU - Zhang, Yahong
AU  - Zhang Y
AD  - Immunopathology Section, National Institute of Dental and Craniofacial Research, 
      National Institutes of Health, Bethesda, Maryland 20892-4352, USA.
FAU - Wahl, Larry M
AU  - Wahl LM
LA  - eng
GR  - Intramural NIH HHS/United States
PT  - Comparative Study
PT  - Journal Article
PT  - Research Support, N.I.H., Intramural
DEP - 20051021
PL  - England
TA  - J Leukoc Biol
JT  - Journal of leukocyte biology
JID - 8405628
RN  - 0 (Anti-Inflammatory Agents, Non-Steroidal)
RN  - 0 (Antibodies, Monoclonal)
RN  - 0 (CCL2 protein, human)
RN  - 0 (Chemokine CCL2)
RN  - 0 (Lipoproteins, LDL)
RN  - 0 (Oxytocics)
RN  - 0 (Tumor Necrosis Factor-alpha)
RN  - 0 (oxidized low density lipoprotein)
RN  - 83869-56-1 (Granulocyte-Macrophage Colony-Stimulating Factor)
RN  - 9007-41-4 (C-Reactive Protein)
RN  - EC 3.4.24.7 (Matrix Metalloproteinase 1)
RN  - K7Q1JQR04M (Dinoprostone)
RN  - XXE1CET956 (Indomethacin)
SB  - IM
MH  - Anti-Inflammatory Agents, Non-Steroidal/pharmacology
MH  - Antibodies, Monoclonal/immunology/pharmacology
MH  - C-Reactive Protein/immunology/*pharmacology
MH  - Cell Movement/drug effects/immunology
MH  - Cells, Cultured
MH  - Chemokine CCL2/immunology/*pharmacology
MH  - Coronary Artery Disease/enzymology/immunology/pathology
MH  - Dinoprostone/immunology/*pharmacology
MH  - Drug Synergism
MH  - Gene Expression Regulation, Enzymologic/drug effects/immunology
MH  - Granulocyte-Macrophage Colony-Stimulating Factor/immunology/pharmacology
MH  - Humans
MH  - Indomethacin/pharmacology
MH  - Lipoproteins, LDL/immunology/*pharmacology
MH  - Macrophage Activation/drug effects/immunology
MH  - Matrix Metalloproteinase 1/immunology/*metabolism
MH  - Monocytes/*enzymology/immunology/pathology
MH  - Oxytocics/immunology/*pharmacology
MH  - Tumor Necrosis Factor-alpha/immunology/pharmacology
EDAT- 2005/10/26 09:00
MHDA- 2006/03/03 09:00
CRDT- 2005/10/26 09:00
PHST- 2005/10/26 09:00 [pubmed]
PHST- 2006/03/03 09:00 [medline]
PHST- 2005/10/26 09:00 [entrez]
AID - jlb.0505241 [pii]
AID - 10.1189/jlb.0505241 [doi]
PST - ppublish
SO  - J Leukoc Biol. 2006 Jan;79(1):105-13. doi: 10.1189/jlb.0505241. Epub 2005 Oct 21.