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Thrombin preconditioning attenuates iron-induced neuronal death.

Haitao Hu1, Shiro Yamashita, Shuijiang Song

  • 1Department of Neurosurgery, University of Michigan, Ann Arbor, MI, USA.

Acta Neurochirurgica. Supplement
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Summary

Thrombin preconditioning (TPC) protects cultured neurons from iron-induced death. This neuroprotection involves protease-activated receptors (PARs) and the p44/42 MAPK/p70S6K pathway.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Intracerebral hemorrhage (ICH) and cerebral ischemia can cause brain injury.
  • Thrombin preconditioning (TPC) is a phenomenon where low-dose thrombin pretreatment attenuates brain injury.

Purpose of the Study:

  • To investigate if TPC reduces iron-induced neuronal death in cultured neurons.
  • To examine the roles of protease-activated receptors (PARs) and the p44/42 mitogen-activated protein kinase (p44/42MAPK)/70-kDa ribosomal protein S6 kinase (p70S6K) signaling pathway in TPC.

Main Methods:

  • Primary cultured neurons were pretreated with vehicle, thrombin, or PAR agonists, followed by iron exposure.
  • Lactate dehydrogenase (LDH) was measured to assess cell death.
  • Western blotting was used to analyze protein levels of activated p44/42MAPK and p70S6K.
  • The effect of PD098059, a p44/42MAPK inhibitor, on TPC was evaluated.

Main Results:

  • TPC and PAR agonist pretreatment significantly reduced iron-induced neuronal death.
  • Thrombin upregulated activated p44/42MAPK and p70S6K protein levels, an effect blocked by PPACK (a thrombin inhibitor).
  • PD098059 abolished the neuroprotective effect of TPC against iron.

Conclusions:

  • TPC confers neuroprotection against iron-induced neuronal death.
  • This protective effect is mediated through the activation of PARs and the p44/42MAPK/p70S6K signaling pathway.