Subtoxic levels of hydrogen peroxide induce brain-derived neurotrophic factor expression to protect PC12 cells

BMC Research Notes

Taku Nedachi¹  Hideo Kawaguchi¹  Kotaro Fujino²  Sei Imura¹  Nanako Kobayashi¹  Ken-Ichi Kawashima²  Kazunori Sato²  Yurina Ogura² 

[1] Faculty of Life Sciences, Toyo University, 1-1-1 Izumino, Itakura-machi, Oura-gun, Gunma 374-0193, Japan;Department of Life Sciences, Graduate School of Life Sciences, Toyo University, 1-1-1 Izumino, Itakura-machi, Oura-gun, Gunma 374-0193, Japan

关键词: Cell death;    PC12 cells;    BDNF;    Oxidative stress;   

Others  :  1118236
DOI  :  10.1186/1756-0500-7-840

 received in 2014-07-08, accepted in 2014-11-18,  发布年份 2014

【 摘 要 】

Background

Oxidative stress is one of the mechanisms underlying pathogenesis in neurodegenerative diseases such as Alzheimer’s disease. Generally, oxidative stress represents cell toxicity; however, we recently found that oxidative stress promotes the expression of growth factor progranulin (PGRN) in HT22 murine hippocampus cells, thereby protecting the HT22 cells. In this study, we attempted to clarify whether a similar system exists in the other neuronal cell model, rat pheochromocytoma (PC12) cells.

Results

After confirming that high concentrations of hydrogen peroxide (H₂O₂; 100–250 μM) initiate PC12 cell death, we analyzed growth factor expressional changes after H₂O₂ treatment. We found, intriguingly, that gene expression of brain-derived neurotrophic factor (BDNF), but not PGRN was significantly induced by H₂O₂. Although little expression of the high affinity BDNF receptor tropomyosin-related kinase TrkB was observed in PC12 cells, expression of low affinity neurotrophin receptor, p75NTR, was clearly observed. This BDNF signaling appeared to contribute to PC12 cell protection, since PC12 cell death was significantly attenuated by BDNF treatment.

Conclusions

Based on our results, we conclude that the induction of BDNF by subtoxic levels of H₂O₂ and its signaling may have roles in PC12 cell protection.

【 授权许可】

   
2014 Ogura et al.; licensee BioMed Central Ltd.

【 图 表 】

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