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Brain Inj. 2016;30(9):1150-9. doi: 10.3109/02699052.2016.1161828. Epub 2016 May 31.

Effects of PTEN inhibition on the regulation of Tau phosphorylation in rat cortical neuronal injury after oxygen and glucose deprivation.

Zhao J1,2, Chen Y1,2, Xu Y2, Pi G2.

Author information

1
a Department of Neonatology , Affiliated Hospital of North Sichuan Medical College , Nanchong , PR China.
2
b Department of Pediatrics , North Sichuan Medical College , Nanchong , PR China.

Abstract

OBJECTIVE:

This report investigated the involvement of the PTEN pathway in the regulation of Tau phosphorylation using an oxygen and glucose deprivation (OGD) model with rat cortical neurons.

METHODS:

Primary cortical neurons were used to establish the oxygen and glucose deprivation (OGD) model in vitro. These were randomly divided into control, OGD, bpV+OGD, As+OGD, Se+OGD and Mock treatment groups. The neuron viability was assessed by MTT, the cell apoptosis was detected using TUNEL staining. The expression of Phospho-PTEN/PTEN, Phospho-Tau/Tau, Phospho-Akt/Akt and Phospho-GSK-3β/GSK-3β were detected by Western blotting.

RESULTS:

OGD induced Tau phosphorylation through PTEN and glycogen synthase kinase-3β (GSK-3β) activation, together with a decrease in AKT activity. Pre-treatment with bpv, a potent PTEN inhibitor, and PTEN antisense nucleotides decreased PTEN and GSK-3β activity and caused alterations in Tau phosphorylation. Neuronal apoptosis was also reduced.

CONCLUSIONS:

The PTEN/Akt/GSK-3β/Tau pathway is involved in the regulation of neuronal injury, providing a novel route for protecting neurons following neonatal HI.

KEYWORDS:

Akt; Neuron; PTEN; hypoxia-ischaemia; oxygen and glucose deprivation; signalling pathway; tau

PMID:
27245882
DOI:
10.3109/02699052.2016.1161828
[Indexed for MEDLINE]

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