Thrombin-thrombomodulin activation of protein C facilitates the activation of progelatinase A

FEBS Lett. 2001 Apr 6;494(1-2):129-32. doi: 10.1016/s0014-5793(01)02296-7.

Abstract

The activation of the matrix metalloproteinase progelatinase A (MMP-2) has been of keen interest because an increase in MMP-2 activity has been implicated in disease states such as cancer and atherosclerosis. Activation of MMP-2 occurs on the surface of specific cell types in two steps. In the first step, primary cleavage of MMP-2 by a membrane-type matrix metalloproteinase generates an intermediate. A secondary cleavage and activation of the intermediate is thought to occur autocatalytically. Previous studies have shown that thrombin can also activate progelatinase A in the presence of endothelial cells. We show that this cell-dependent mechanism of MMP-2 activation also occurs with THP-1 cells and involves binding of thrombin to thrombomodulin present on the cell surface and generation of the anti-coagulant protein, activated protein C. We demonstrate that activated protein C is directly responsible for activation and cleavage of the gelatinase A intermediate. This work contributes new mechanistic insights into the activation of MMP-2 and provides a novel link between matrix metalloproteinase activation and anti-coagulation.

Publication types

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

MeSH terms

  • Cell Line
  • Cells, Cultured
  • Endothelium, Vascular / cytology
  • Enzyme Activation
  • Enzyme Precursors / metabolism*
  • Gelatinases / metabolism*
  • Humans
  • Metalloendopeptidases / metabolism*
  • Protein C / metabolism*
  • Thrombin / metabolism*
  • Thrombomodulin / metabolism*

Substances

  • Enzyme Precursors
  • Protein C
  • Thrombomodulin
  • Thrombin
  • Gelatinases
  • Metalloendopeptidases
  • progelatinase