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Metallothionein-III provides neuronal protection through activation of nuclear factor-κB via the TrkA/phosphatidylinositol-3 kinase/Akt signaling pathway
- Metallothionein-III provides neuronal protection through activation of nuclear factor-κB via the TrkA/phosphatidylinositol-3 kinase/Akt signaling pathway
- Kim H.G.; Hwang Y.P.; Han E.H.; Choi C.Y.; Yeo C.-Y.; Kim J.Y.; Lee K.Y.; Jeong H.G.
- Ewha Authors
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- Journal Title
- Toxicological Sciences
- Toxicological Sciences vol. 112, no. 2, pp. 435 - 449
- SCI; SCIE; SCOPUS
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- Metallothionein (MT)-III is associated with resistance to neuronal injury. However, the underlying mechanism for its effects is unclear. The present study investigated the mechanisms of MT-III protection of neuronal cells from hypoxia or DNA damage-induced cell death. MT-III reduced the hydrogen peroxide-or DNA damage-induced effects on neuronal cells, including the cell death, the activation of caspase-3 and -9, and the release of mitochondrial cytochrome c to the cytoplasm in a dose-dependent manner. MT-III also increased the activation of Akt, the phosphorylation and degradation of IκB, the nuclear translocation/accumulation and the transcriptional activity of nuclear factor-κB (NF-κB) in neuronal cells in a dose-dependent manner. The MT-III-induced antiapoptotic effects and increase in NF-κB activity were blocked by specific inhibitors of TrkA, phosphatidylinositol-3 kinase (PI3K), Akt, or NF-κB, indicating that MT-III provides neuronal protection by activating NF-κB through the TrkA/PI3K/Akt signaling pathway. © The Author 2009. Published by Oxford University Press on behalf of the Society of Toxicology. All rights reserved. For permissions, please email: email@example.com.
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