Fc-gamma receptor cross-linking by immune complexes induces matrix metalloproteinase-1 in U937 cells via mitogen-activated protein kinase

Arterioscler Thromb Vasc Biol. 2000 Dec;20(12):2533-8. doi: 10.1161/01.atv.20.12.2533.

Abstract

Matrix metalloproteinase-1 (MMP-1) secreted by macrophages potentially contributes to plaque rupture. Because large quantities of immunoglobulin G and ICs (ICs), including low density lipoprotein-containing ICs (LDL-ICs), are present in atherosclerotic lesions, we examined the effect of LDL-ICs on macrophage MMP-1 expression. With the use of ICs prepared with human LDL and rabbit anti-LDL antiserum, our enzyme-linked immunosorbent assays and Northern blots showed that MMP-1 secretion and expression by U937 histiocytes were induced by LDL-ICs. Furthermore, our results showed that blocking of Fc-gamma receptor I and II (FcgammaRI and FcgammaRII) inhibited 70% and 55%, respectively, of the LDL-IC-induced secretion of MMP-1. Finally, our data showed that both PD98059, an inhibitor of the mitogen-activated protein kinase pathway, and Ro-31-2880, an inhibitor of protein kinase C, inhibited LDL-IC-stimulated MMP-1 secretion in a dose-dependent manner, with 96% and 95% inhibition, respectively, at the respective doses of 50 micromol/L and 80 nmol/L. In conclusion, this study demonstrated for the first time that LDL-ICs induce macrophage MMP-1 secretion by cocross-linking FcgammaRI and FcgammaRII and triggering a protein kinase C-dependent mitogen-activated protein kinase pathway. These results suggest that LDL-ICs and other ICs localized in atherosclerotic plaques may be potent stimulators for macrophage MMP-1 expression and may contribute to plaque rupture and acute coronary events.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Antibodies, Anti-Idiotypic / immunology
  • Antibodies, Monoclonal / pharmacology
  • Antigen-Antibody Complex / immunology*
  • Antigen-Antibody Complex / pharmacology
  • Antigens, CD / immunology*
  • Arteriosclerosis / enzymology
  • Arteriosclerosis / immunology
  • Collagenases / analysis
  • Dose-Response Relationship, Drug
  • Enzyme Inhibitors / pharmacology
  • Enzyme-Linked Immunosorbent Assay
  • Flavonoids / pharmacology
  • Humans
  • Immunoglobulin G / immunology
  • Immunoglobulin G / pharmacology
  • Lipoproteins, LDL / immunology*
  • Lipoproteins, LDL / pharmacology
  • Macrophages / drug effects
  • Macrophages / enzymology*
  • Matrix Metalloproteinase 1 / biosynthesis
  • Matrix Metalloproteinase 1 / metabolism*
  • Mitogen-Activated Protein Kinases / antagonists & inhibitors
  • Mitogen-Activated Protein Kinases / metabolism
  • Protein Kinase C / antagonists & inhibitors
  • Protein Kinase C / metabolism
  • Receptors, IgG / antagonists & inhibitors
  • Receptors, IgG / immunology*
  • Tissue Inhibitor of Metalloproteinase-1 / antagonists & inhibitors
  • Tissue Inhibitor of Metalloproteinase-1 / metabolism
  • U937 Cells

Substances

  • Antibodies, Anti-Idiotypic
  • Antibodies, Monoclonal
  • Antigen-Antibody Complex
  • Antigens, CD
  • Enzyme Inhibitors
  • Fc gamma receptor IIA
  • Flavonoids
  • Immunoglobulin G
  • Lipoproteins, LDL
  • Receptors, IgG
  • Tissue Inhibitor of Metalloproteinase-1
  • anti-IgG
  • oxidized low density lipoprotein
  • Protein Kinase C
  • Mitogen-Activated Protein Kinases
  • Collagenases
  • Matrix Metalloproteinase 1
  • 2-(2-amino-3-methoxyphenyl)-4H-1-benzopyran-4-one