Journal
CNS NEUROSCIENCE & THERAPEUTICS
Volume 20, Issue 3, Pages 275-281Publisher
WILEY
DOI: 10.1111/cns.12208
Keywords
Mitochondria; Neuroprotection; Stroke; Stem cells; Oxidative stress
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Funding
- NIH NINDS [RO1 1R01NS071956-01]
- James and Esther King Biomedical Research Program [09KB-01-23123, 1KG01-33966]
- USF ORI [HSC-18330, COM HSC-18300]
- USF Department of Neurosurgery and Brain Repair Funds
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Aims DJ-1 is a key redox-reactive neuroprotective protein implicated in regulation of oxidative stress after stroke. However, the molecular mechanism, especially the role of mitochondrial function, by which DJ-1 protects neural cells in stroke remains to be elucidated. The aim of this study was to reveal whether DJ-1 translocates into the mitochondria in exerting neuroprotection against oxidative stress. In particular, we examined DJ-1 secretion from primary rat neural cells (PRNCs) exposed to experimental stroke. Methods Primary rat neural cells were exposed to the oxygen-glucose deprivation (OGD), an established in vitro stroke model, and DJ-1 translocation was measured by immunocytochemistry, and its secretion detected by ELISA. Results Under OGD, DJ-1 translocated into the healthy mitochondria, and significant levels of DJ-1 protein were detected. Treatment with anti-DJ-1 antibody reduced cell viability and mitochondrial activity, and increased glutathione level. Interestingly, OGD reversed the ratio of astrocyte/neuron cells (6/4 to 4/6). Conclusions Altogether, these results revealed that DJ-1 participates in the acute endogenous neuroprotection after stroke via the mitochondrial pathway. That DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offer a new venue for developing neuroprotective and/or neurorestorative strategies against ischemic stroke.
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