Subtoxic levels of hydrogen peroxide induce brain-derived neurotrophic factor expression to protect PC12 cells
Autor: | Taku Nedachi, Yurina Ogura, Hideo Kawaguchi, Nanako Kobayashi, Kotaro Fujino, Sei Imura, Ken-ichi Kawashima, Kazunori Sato |
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Jazyk: | angličtina |
Rok vydání: | 2014 |
Předmět: |
Cell death
Programmed cell death Pathology medicine.medical_specialty medicine.medical_treatment Nerve Tissue Proteins Tropomyosin receptor kinase B Receptors Nerve Growth Factor medicine.disease_cause General Biochemistry Genetics and Molecular Biology Progranulins Neurotrophic factors medicine Animals Receptor trkB Receptors Growth Factor Medicine(all) Brain-derived neurotrophic factor biology Dose-Response Relationship Drug Biochemistry Genetics and Molecular Biology(all) business.industry Growth factor Brain-Derived Neurotrophic Factor PC12 cells General Medicine Hydrogen Peroxide Cell biology Rats Oxidative Stress BDNF nervous system Gene Expression Regulation biology.protein Intercellular Signaling Peptides and Proteins Signal transduction business Oxidative stress Neurotrophin Research Article Signal Transduction |
Zdroj: | BMC Research Notes |
ISSN: | 1756-0500 |
Popis: | 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. |
Databáze: | OpenAIRE |
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