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PTEN deletion prevents ischemic brain injury by activating the mTOR signaling pathway

G D Shi1, Y P OuYang, J G Shi

  • 1Department of Orthopaedics Changzheng Hospital, Second Military Medical University, 415 Fengyang Road, Shanghai 200003, PR China.

Biochemical and Biophysical Research Communications
|December 28, 2010
PubMed

Insights

Inhibiting PTEN (phosphatase and tensin homolog deleted on chromosome 10) protects neurons from death after ischemic brain injury by enhancing mTOR phosphorylation, reducing infarct volume.

Area of Science:

  • Neuroscience
  • Molecular Biology
  • Pathology

Background:

  • The tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) is known to negatively regulate neuronal cell survival.
  • The precise molecular mechanisms by which PTEN influences neuronal cell death, particularly after ischemic events, are not fully elucidated.

Purpose of the Study:

  • To investigate the role of the PTEN/mTOR pathway in neuronal cell death following ischemic brain injury.
  • To determine if inhibiting PTEN can offer neuroprotection against ischemic damage.

Main Methods:

  • Male rats underwent middle cerebral artery occlusion (MCAO) to induce ischemic brain injury.
  • Animals were pretreated with bpv (pic), a PTEN inhibitor, or received intra-cerebroventricular infusion of PTEN siRNA.
  • Infarct volume, TUNEL-positive cells, and levels of mTOR phosphorylation and S6 were assessed.

Main Results:

  • PTEN inhibition with bpv (pic) significantly reduced infarct volume and the number of TUNEL-positive cells, indicating decreased neuronal death.
  • PTEN inhibition prevented the decrease in mTOR phosphorylation and subsequent S6 reduction observed after ischemic injury.
  • Down-regulating PTEN expression via siRNA also decreased neuronal cell death and increased mTOR phosphorylation.

Conclusions:

  • PTEN plays a critical role in regulating neuronal cell death after ischemic brain injury.
  • Inhibition of PTEN confers neuroprotection by maintaining mTOR phosphorylation, thereby preventing neuronal loss.

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