期刊
NEUROSCIENCE
卷 238, 期 -, 页码 242-251出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuroscience.2013.02.046
关键词
neuron; hypoxia-ischemia; signaling pathway; PTEN; GSK-3 beta; CRMP-2
资金
- National Science Foundation of China [30973236, 31171020, 81172174, 81270724]
- Major State Basic Research Development Program [2013CB967404]
- Program of Changjiang Scholars and Innovative Research Team in University [IRT0935]
- Ministry of Education of China [313037, 20110181130002]
- State Commission of Science Technology of China [2012BAI04B04]
- Science and Technology Bureau of Sichuan Province [2010SZ0280]
- Program for Outstanding Young Scholars of Sichuan University [2012SCU04B03]
Alterations in axon-dendrite polarity impair functional recovery in the developing CNS after hypoxia-ischemia (HI) injury. PTEN (phosphatase and tensin homolog deleted on chromosome 10) signaling pathway mediates the formation of neuronal polarity. However, its role in cerebral HI injury is not fully understood. In this study, we investigated the role of PTEN pathway in regulation of axon-dendrite polarity using an oxygen-glucose deprivation (OGD) model with rat cortical neurons. We found that the activity of PTEN and glycogen synthase kinase 313 (GSK-3 beta) was increased after OGD, along with the decrease of the activity in protein kinase B (Akt) and collapsin response mediator protein-2 (CRMP-2). Pretreatment with bpv, a potent inhibitor of PTEN, caused a decrease of the activity in PTEN and GSK-3 beta, and a significant increase of the activity in Akt and CRMP-2. Simultaneously, the morphological polarity of neurons was maintained and neuronal apoptosis was reduced. Moreover, inhibition of PTEN rescued vesicle recycling in axons. These findings suggested that the PTEN/Akt/GSK-3 beta/CRMP-2 pathway is involved in the regulation of axon-dendrite polarity, providing a novel route for protecting neurons following neonatal HI. (C) 2013 IBRO. Published by Elsevier Ltd. All rights reserved.
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