RGD Reference Report - PTEN deletion prevents ischemic brain injury by activating the mTOR signaling pathway. - Rat Genome Database
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PTEN deletion prevents ischemic brain injury by activating the mTOR signaling pathway.

Authors: Shi, GD  OuYang, YP  Shi, JG  Liu, Y  Yuan, W  Jia, LS 
Citation: Shi GD, etal., Biochem Biophys Res Commun. 2011 Jan 28;404(4):941-5. doi: 10.1016/j.bbrc.2010.12.085. Epub 2010 Dec 23.
RGD ID: 10041016
Pubmed: (View Article at PubMed) PMID:21185267
DOI: Full-text: DOI:10.1016/j.bbrc.2010.12.085

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.

Annotation

Disease Annotations    

Objects Annotated

Genes (Rattus norvegicus)
Mtor  (mechanistic target of rapamycin kinase)

Genes (Mus musculus)
Mtor  (mechanistic target of rapamycin kinase)

Genes (Homo sapiens)
MTOR  (mechanistic target of rapamycin kinase)


Additional Information