Oxidized LDL differentially regulates MMP-1 and TIMP-1 expression in vascular endothelial cells

Y Huang1, L Song, S Wu

  • 1Ralph H. Johnson Veterans Administration Medical Center, Charleston, SC 29401, USA. huangyan@musc.edu

Atherosclerosis
|May 23, 2001
PubMed

Insights

Oxidized low-density lipoprotein (oxLDL) reduces Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) in endothelial cells. This imbalance with Matrix Metalloproteinase-1 (MMP-1) may promote atherosclerotic plaque instability.

Area of Science:

  • Cardiovascular Biology
  • Molecular Biology
  • Cell Biology

Background:

  • Oxidized low-density lipoprotein (oxLDL) is implicated in atherosclerosis.
  • oxLDL stimulates Matrix Metalloproteinase-1 (MMP-1) expression in vascular endothelial cells.
  • The role of Tissue Inhibitor of Metalloproteinase-1 (TIMP-1) in oxLDL-mediated effects is unclear.

Purpose of the Study:

  • To investigate the effect of oxLDL on TIMP-1 expression and secretion in human vascular endothelial cells.
  • To compare the regulatory effects of oxLDL and phorbol 12-myristate 13-acetate (PMA) on TIMP-1 and MMP-1.

Main Methods:

  • Enzyme-linked immunosorbent assay (ELISA) for protein secretion.
  • Northern blot analysis for gene expression.
  • Enzymatic activity assay for collagenase activity.

Main Results:

  • oxLDL significantly inhibited TIMP-1 secretion and expression in human umbilical vein endothelial cells and human aortic endothelial cells.
  • PMA stimulated both TIMP-1 and MMP-1 expression and secretion.
  • oxLDL increased MMP-1 expression and secretion, and elevated collagenase activity.
  • oxLDL induced differential regulation of TIMP-1 and MMP-1, unlike PMA's coordinate regulation.

Conclusions:

  • oxLDL differentially regulates TIMP-1 and MMP-1 in vascular endothelial cells.
  • The uncoordinated regulation by oxLDL leads to increased collagen degradation.
  • This imbalance may contribute to atherosclerotic plaque destabilization.