Smad3-dependent induction of plasminogen activator inhibitor-1 in astrocytes mediates neuroprotective activity of transforming growth factor-beta 1 against NMDA-induced necrosis

Mol Cell Neurosci. 2002 Dec;21(4):634-44. doi: 10.1006/mcne.2002.1206.

Abstract

The intravenous injection of the serine protease, tissue-type plasminogen activator (t-PA), has shown to benefit stroke patients by promoting early reperfusion. However, it has recently been suggested that t-PA activity, in the cerebral parenchyma, may also potentiate excitotoxic neuronal death. The present study has dealt with the role of the t-PA inhibitor, PAI-1, in the neuroprotective activity of the cytokine TGF-beta1 and focused on the transduction pathway involved in this effect. We demonstrated that PAI-1, produced by astrocytes, mediates the neuroprotective activity of TGF-beta 1 against N-methyl-D-aspartate (NMDA) receptor-mediated excitotoxicity. This t-PA inhibitor, PAI-1, protected neurons against NMDA-induced neuronal death by modulating the NMDA-evoked calcium influx. Finally, we showed that the activation of the Smad3-dependent transduction pathway mediates the TGF-beta-induced up-regulation of PAI-1 and subsequent neuroprotection. Overall, this study underlines the critical role of the t-PA/PAI-1 axis in the regulation of glutamatergic neurotransmission.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Animals, Newborn
  • Astrocytes / drug effects*
  • Astrocytes / metabolism
  • Brain / drug effects
  • Brain / metabolism
  • Brain / physiopathology
  • Calcium Signaling / drug effects
  • Calcium Signaling / physiology
  • Cells, Cultured
  • Coculture Techniques
  • DNA-Binding Proteins / drug effects
  • DNA-Binding Proteins / metabolism*
  • Dose-Response Relationship, Drug
  • Excitatory Amino Acid Antagonists / pharmacology
  • Fetus
  • Mice
  • N-Methylaspartate / antagonists & inhibitors*
  • Nerve Degeneration / chemically induced
  • Nerve Degeneration / drug therapy
  • Nerve Degeneration / metabolism
  • Neurons / drug effects
  • Neurons / metabolism
  • Neuroprotective Agents / metabolism*
  • Neuroprotective Agents / pharmacology
  • Neurotoxins / antagonists & inhibitors*
  • Plasminogen Activator Inhibitor 1 / genetics
  • Plasminogen Activator Inhibitor 1 / metabolism*
  • Plasminogen Activator Inhibitor 1 / pharmacology
  • Recombinant Fusion Proteins
  • Smad3 Protein
  • Stroke / drug therapy
  • Stroke / metabolism
  • Stroke / physiopathology
  • Tissue Plasminogen Activator / antagonists & inhibitors
  • Tissue Plasminogen Activator / therapeutic use
  • Tissue Plasminogen Activator / toxicity
  • Trans-Activators / drug effects
  • Trans-Activators / metabolism*
  • Transforming Growth Factor beta / metabolism*
  • Transforming Growth Factor beta / pharmacology
  • Transforming Growth Factor beta1

Substances

  • DNA-Binding Proteins
  • Excitatory Amino Acid Antagonists
  • Neuroprotective Agents
  • Neurotoxins
  • Plasminogen Activator Inhibitor 1
  • Recombinant Fusion Proteins
  • Smad3 Protein
  • Smad3 protein, mouse
  • Tgfb1 protein, mouse
  • Trans-Activators
  • Transforming Growth Factor beta
  • Transforming Growth Factor beta1
  • N-Methylaspartate
  • Tissue Plasminogen Activator