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
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