The hemopexin domain of matrix metalloproteinase-9 activates cell signaling and promotes migration of schwann cells by binding to low-density lipoprotein receptor-related protein

J Neurosci. 2008 Nov 5;28(45):11571-82. doi: 10.1523/JNEUROSCI.3053-08.2008.

Abstract

Low-density lipoprotein receptor-related protein (LRP-1) is an endocytic receptor for diverse proteins, including matrix metalloproteinase-9 (MMP-9), and a cell-signaling receptor. In the peripheral nervous system (PNS), LRP-1 is robustly expressed by Schwann cells only after injury. Herein, we demonstrate that MMP-9 activates extracellular-signal-regulated kinase (ERK1/2) and Akt in Schwann cells in culture. MMP-9 also promotes Schwann cell migration. These activities require LRP-1. MMP-9-induced cell signaling and migration were blocked by inhibiting MMP-9-binding to LRP-1 with receptor-associated protein (RAP) or by LRP-1 gene silencing. The effects of MMP-9 on Schwann cell migration also were inhibited by blocking the cell-signaling response. An antibody targeting the hemopexin domain of MMP-9, which mediates the interaction with LRP-1, blocked MMP-9-induced cell signaling and migration. Furthermore, a novel glutathione-S-transferase fusion protein (MMP-9-PEX), which includes only the hemopexin domain of MMP-9, replicated the activities of intact MMP-9, activating Schwann cell signaling and migration by an LRP-1-dependent pathway. Constitutively active MEK1 promoted Schwann cell migration; in these cells, MMP-9-PEX had no further effect, indicating that ERK1/2 activation is sufficient to explain the effects of MMP-9-PEX on Schwann cell migration. Injection of MMP-9-PEX into sciatic nerves, 24 h after crush injury, robustly increased phosphorylation of ERK1/2 and Akt. This response was inhibited by RAP. MMP-9-PEX failed to activate cell signaling in uninjured nerves, consistent with the observation that Schwann cells express LRP-1 at significant levels only after nerve injury. These results establish LRP-1 as a cell-signaling receptor for MMP-9, which may be significant in regulating Schwann cell migration and physiology in PNS injury.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Cell Death / drug effects
  • Cell Movement / drug effects*
  • Cell Movement / physiology
  • Cells, Cultured
  • Drug Interactions
  • Enzyme Inhibitors / pharmacology
  • Gene Expression Regulation / drug effects
  • Gene Expression Regulation / physiology
  • Hemopexin / metabolism*
  • LDL-Receptor Related Protein-Associated Protein / physiology*
  • Matrix Metalloproteinase 9 / metabolism
  • Matrix Metalloproteinase 9 / pharmacology*
  • Mitogen-Activated Protein Kinase 3 / metabolism
  • Neuregulin-1 / pharmacology
  • Oncogene Protein v-akt / metabolism
  • Protein Interaction Domains and Motifs / drug effects
  • Protein Interaction Domains and Motifs / physiology
  • RNA, Small Interfering / pharmacology
  • Rats
  • Schwann Cells / cytology*
  • Schwann Cells / physiology*
  • Sciatic Nerve / cytology
  • Sciatic Neuropathy / metabolism
  • Signal Transduction / drug effects*
  • Signal Transduction / physiology
  • rap GTP-Binding Proteins / pharmacology

Substances

  • Enzyme Inhibitors
  • LDL-Receptor Related Protein-Associated Protein
  • Neuregulin-1
  • RNA, Small Interfering
  • Hemopexin
  • Oncogene Protein v-akt
  • Mitogen-Activated Protein Kinase 3
  • Matrix Metalloproteinase 9
  • rap GTP-Binding Proteins