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Akt/Bad signaling and motor neuron survival after spinal cord injury

Fengshan Yu1, Taku Sugawara, Carolina M Maier

  • 1Department of Neurosurgery, Stanford University School of Medicine, Stanford, CA 94305, USA.

Neurobiology of Disease
|May 18, 2005
PubMed

Insights

The Akt/Bad signaling pathway promotes motor neuron survival after spinal cord injury (SCI). Oxidative stress influences this pathway, suggesting therapeutic targets for SCI recovery.

Area of Science:

  • Neuroscience
  • Cellular Signaling
  • Molecular Biology

Background:

  • The Akt/Bad pathway promotes cell survival in cerebral ischemia by inactivating proapoptotic Bad.
  • The role of the Akt/Bad pathway in spinal cord injury (SCI) remains unclear.

Purpose of the Study:

  • To investigate the involvement of the Akt/Bad signaling pathway in motor neuron survival following SCI.
  • To explore the influence of oxidative stress on this pathway in the context of SCI.

Main Methods:

  • Western blotting to detect phospho-Akt and phospho-Bad levels.
  • Immunohistochemistry to assess colocalization in motor neurons.
  • PI3-K inhibition to study pathway modulation.
  • Analysis of Bad dimerization and binding partners (14-3-3, Bcl-XL).
  • Comparison between SOD1-overexpressing rats and wild-type rats after SCI.

Main Results:

  • Phospho-Akt and phospho-Bad were upregulated 1 day post-SCI and colocalized in surviving motor neurons.
  • PI3-K inhibition decreased phospho-Akt and phospho-Bad expression.
  • SCI increased cytosolic Bad/14-3-3 binding and decreased mitochondrial Bad/Bcl-XL binding.
  • SOD1 overexpression in rats enhanced Akt/Bad signaling and altered binding patterns compared to wild-type rats post-SCI.

Conclusions:

  • The Akt/Bad signaling pathway is activated in motor neurons after SCI, contributing to their survival.
  • Oxidative stress appears to modulate the Akt/Bad pathway and impact motor neuron survival following SCI.

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