Journal
NEUROBIOLOGY OF DISEASE
Volume 62, Issue -, Pages 56-61Publisher
ACADEMIC PRESS INC ELSEVIER SCIENCE
DOI: 10.1016/j.nbd.2013.09.007
Keywords
Stroke; Mitochondria; Stem cells; Cell death; Neuroprotection
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Funding
- NIH NINDS [RO1 1R01NS071956-01]
- James and Esther King Biomedical Research Program [09KB-01-23123]
- USF ORI [HSC-18330]
- COM [HSC-18300]
- USF Department of Neurosurgery and Brain Repair Funds
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DJ-1 is an important redox-reactive neuroprotective protein implicated in regulation of oxidative stress after ischemia. However the molecular mechanism, especially the mitochondrial function, by which DJ-1 protects neuronal 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 an in vitro model of stroke. Human neural progenitor cells (hNPCs) were initially exposed to oxygen-glucose deprivation and reperfusion injury, and thereafter, DJ-1 translocation was measured by immunocytochemistry and its secretion by hNPCs was detected by enzyme-linked immunosorbant assay (ELISA). Exposure of hNPCs to experimental stroke injury resulted in DJ-1 translocation into the mitochondria. Moreover, significant levels of DJ-1 protein were secreted by the injured hNPCs. Our findings revealed that DJ-1 principally participates in the early phase of stroke involving the mitochondrial pathway. DJ-1 was detected immediately after stroke and efficiently translocated into the mitochondria offering a new venue for developing treatment strategies against ischemic stroke. (C) 2013 Published by Elsevier Inc.
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