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J Biol Chem, Vol. 274, Issue 17, 11924-11929, April 23, 1999
From the We investigated whether inflammatory cytokines or
oxidized low density lipoproteins (Ox-LDL) present in human atheroma
modulate extracellular matrix degradation by inducing membrane type
1-matrix metalloproteinase (MT1-MMP) expression. Cultured human
endothelial cells (EC) constitutively expressed MT1-MMP mRNA and
protein with enzymatic activity. Tumor necrosis factor-
Inflammatory Cytokines and Oxidized Low Density Lipoproteins
Increase Endothelial Cell Expression of Membrane Type 1-Matrix
Metalloproteinase
§¶,,,,, and Atherosclerosis Research Center, Division of
Cardiology, Cedars-Sinai Medical Center, UCLA School of Medicine, Los
Angeles, California 90048, the § Harbor-UCLA Medical Center,
Torrance, California 90502, and the ¶ Vascular Medicine and
Atherosclerosis Unit, Brigham and Women's Hospital, Harvard Medical
School, Boston, Massachusetts 02115
(TNF-),
interleukin-1, or interleukin-1
caused a
time-dependent increase in the steady-state MT1-MMP
mRNA levels within 4 h of exposure, peaking about 4-fold by
6 h, and remaining elevated for 12 h. Increased MT1-MMP
mRNA correlated with a 2.5-fold increase in MT1-MMP protein in EC
membranes. Ox-LDL also increased MT1-MMP mRNA levels that varied
with the duration of exposure and degree of LDL oxidation. The increase in MT1-MMP mRNA occurred within 6 h of exposure to Ox-LDL and peaked over 3-fold by 6 h. Ox-LDL, but not native LDL, increased MT1-MMP protein by 2-fold in EC membranes. A combination of TNF- and
Ox-LDL was additive in increasing MT1-MMP expression. Nuclear run-on
assays showed that TNF- or Ox-LDL augmented steady-state mRNA
levels by increased transcription of the MT1-MMP gene. These findings
indicate that activation of EC by inflammatory cytokines and/or Ox-LDL
increase MT1-MMP expression. Since MT1-MMP promotes matrix degradation
by activating pro-MMP-2, these results suggest a novel mechanism
whereby cytokines or Ox-LDL may influence extracellular matrix remodeling.
Copyright © 1999 by The American Society for Biochemistry and Molecular Biology, Inc.
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