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

Biochem Biophys Res Commun. 2011 Jan 28;404(4):941-5. doi: 10.1016/j.bbrc.2010.12.085. Epub 2010 Dec 23.

Abstract

It is increasingly clear that the tumor suppressor PTEN (phosphatase and tensin homolog deleted on chromosome 10) is a negative regulator of neuronal cell survival. However, its molecular mechanisms remain poorly understood. Here we found that PTEN/mTOR is critical for controlling neuronal cell death after ischemic brain injury. Male rats were subjected to MCAO (middle cerebral artery occlusion) followed by pretreating with bpv (pic), a potent inhibitor for PTEN, or by intra-cerebroventricular infusion of PTEN siRNA. bpv (pic) significantly decreased infarct volume and reduced the number of TUNEL-positive cells. We further demonstrated that although bpv (pic) did not affect brain injury-induced mTOR protein expression, bpv (pic) prevented decrease in phosphorylation of mTOR, and the subsequent decrease in S6. Similarly, down-regulation of PTEN expression also reduced the number of TUNEL-positive cells, and increased phospho-mTOR. These data suggest that PTEN deletion prevents neuronal cell death resulting from ischemic brain injury and that its neuroprotective effects are mediated by increasing the injury-induced mTOR phosphorylation.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Apoptosis / genetics*
  • Brain Infarction / enzymology
  • Brain Infarction / genetics
  • Brain Infarction / pathology
  • Brain Ischemia / enzymology
  • Brain Ischemia / genetics
  • Brain Ischemia / pathology*
  • Disease Models, Animal
  • Down-Regulation
  • Gene Deletion
  • Male
  • Neurons / enzymology
  • Neurons / pathology*
  • Organometallic Compounds / pharmacology
  • PTEN Phosphohydrolase / antagonists & inhibitors
  • PTEN Phosphohydrolase / genetics
  • PTEN Phosphohydrolase / metabolism*
  • Phosphorylation
  • Rats
  • Signal Transduction
  • TOR Serine-Threonine Kinases / metabolism*

Substances

  • Organometallic Compounds
  • oxodiperoxo(pyridine-2-carboxylate)vanadate(V)
  • mTOR protein, rat
  • TOR Serine-Threonine Kinases
  • PTEN Phosphohydrolase
  • Pten protein, rat