| First Author | Fukui K | Year | 2019 |
| Journal | J Clin Biochem Nutr | Volume | 64 |
| Issue | 1 | Pages | 36-44 |
| PubMed ID | 30705510 | Mgi Jnum | J:352472 |
| Mgi Id | MGI:7707340 | Doi | 10.3164/jcbn.18-31 |
| Citation | Fukui K, et al. (2018) Proteomic study on neurite responses to oxidative stress: search for differentially expressed proteins in isolated neurites of N1E-115 cells. J Clin Biochem Nutr 64(1):36-44 |
| abstractText | Reactive oxygen species attack several living organs and induce cell death. Previously, we found axonal/dendrite degeneration before the induction of cell death in hydrogen peroxide-treated neuroblastoma: N1E-115 cells and primary neurons. This phenomenon may be connected with membrane oxidation, microtubule destabilization and disruption of intracellular calcium homeostasis. However, its detailed mechanisms are not fully understood. Here, we identified proteins after treatment with hydrogen peroxide using isolated neurites by liquid chromatography-matrix-assisted laser desorption/ionization-time of flight/time of flight analysis. Twenty-one proteins were increased after treatment with hydrogen peroxide. Specifically, 5 proteins which were secretogranin-1, heat shock protein family D member 1, Brain acid soluble protein 1, heat shock 70-kDa protein 5 and superoxide dismutase 1, were identified of all experiments and increased in isolated neurites of hydrogen peroxide-treated cells compared to the controls. Furthermore, secretogranin-1 and heat shock protein family D member 1 protein expressions were significantly increased in normal aged and Alzheimer''s transgenic mice brains. These results indicate that secretogranin-1 and heat shock protein family D member 1 might contribute to reactive oxygen species-induced neurite degeneration. Both proteins have been related to neurodegenerative disorders, so their study may shed light on neurite dysfunction. |
