| First Author | Kim HG | Year | 2009 |
| Journal | Toxicol Sci | Volume | 112 |
| Issue | 2 | Pages | 435-49 |
| PubMed ID | 19767621 | Mgi Jnum | J:155004 |
| Mgi Id | MGI:4412136 | Doi | 10.1093/toxsci/kfp230 |
| Citation | Kim HG, et al. (2009) Metallothionein-III provides neuronal protection through activation of nuclear factor-kappaB via the TrkA/phosphatidylinositol-3 kinase/Akt signaling pathway. Toxicol Sci 112(2):435-49 |
| abstractText | 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 IkappaB, the nuclear translocation/accumulation and the transcriptional activity of nuclear factor-kappaB (NF-kappaB) in neuronal cells in a dose-dependent manner. The MT-III-induced antiapoptotic effects and increase in NF-kappaB activity were blocked by specific inhibitors of TrkA, phosphatidylinositol-3 kinase (PI3K), Akt, or NF-kappaB, indicating that MT-III provides neuronal protection by activating NF-kappaB through the TrkA/PI3K/Akt signaling pathway. |
