Journal
NEUROSCIENCE LETTERS
Volume 450, Issue 1, Pages 45-50Publisher
ELSEVIER IRELAND LTD
DOI: 10.1016/j.neulet.2008.11.011
Keywords
Akt; H2O2; p62; PDK1; Survival; 14-3-3 theta
Categories
Funding
- Korea Research 276 Foundation to IJ [KRF 2006-C00157]
- MOHW [A04-0018-AY1204-07M4-00020B]
- MOST [M103KV010007-06K2201-00710]
- National Research Foundation of Korea [22-2009-00-001-00] Funding Source: Korea Institute of Science & Technology Information (KISTI), National Science & Technology Information Service (NTIS)
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The p62 protein has been identified as a major component of the protein aggregations associated with neurodegenerative disease. Oxidative insult has also been identified as a principal cause of neurodegenerative disease. Thus, in the present study, we investigated the potential role of p62 in oxidative stress-induced cell death in SH-SY5Y human neuroblastoma cells. The results indicated that H2O2 treatment induced p62 expression in SH-SY5Y cells. In addition, p62 showed neuroprotective effects against H2O2-induced cell death in differentiated SH-SY5Y cells. p62 expression prolonged Akt phosphorylation during the later stages of H2O2-induced cell death. Furthermore, coexpression of p62 and wild-type PDK1. the upstream kinase of Akt, further increased Akt phosphorylation and cell viability. whereas the expression of kinase-defective PDK1 reversed the cytoprotective effects of p62 under oxidative stress. Overexpression of p62 led to the dissociation of PDK1 from the 14-3-3 theta protein, which is thought to be a negative regulator of PDK1 kinase activity. These findings suggest a mechanism that involves the p62-mediated modulation Of the interaction between signaling molecules and results in cell survival. (c) 2008 Elsevier Ireland Ltd. All rights reserved.
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