{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,29]],"date-time":"2026-05-29T20:32:49Z","timestamp":1780086769478,"version":"3.54.0"},"reference-count":48,"publisher":"Wiley","issue":"3","license":[{"start":{"date-parts":[[2013,12,30]],"date-time":"2013-12-30T00:00:00Z","timestamp":1388361600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/creativecommons.org\/licenses\/by-nc-nd\/3.0\/"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["CNS Neurosci Ther"],"published-print":{"date-parts":[[2014,3]]},"abstract":"<jats:title>Summary<\/jats:title><jats:sec><jats:title>Aims<\/jats:title><jats:p><jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 is a key redox\u2010reactive neuroprotective protein implicated in regulation of oxidative stress after stroke. However, the molecular mechanism, especially the role of mitochondrial function, by which <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 protects neural cells in stroke remains to be elucidated. The aim of this study was to reveal whether <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 translocates into the mitochondria in exerting neuroprotection against oxidative stress. In particular, we examined <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 secretion from primary rat neural cells (<jats:styled-content style=\"fixed-case\">PRNC<\/jats:styled-content>s) exposed to experimental stroke.<\/jats:p><\/jats:sec><jats:sec><jats:title>Methods<\/jats:title><jats:p>Primary rat neural cells were exposed to the oxygen\u2013glucose deprivation (<jats:styled-content style=\"fixed-case\">OGD<\/jats:styled-content>), an established <jats:italic>in vitro<\/jats:italic> stroke model, and <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 translocation was measured by immunocytochemistry, and its secretion detected by <jats:styled-content style=\"fixed-case\">ELISA<\/jats:styled-content>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>Under <jats:styled-content style=\"fixed-case\">OGD<\/jats:styled-content>,<jats:styled-content style=\"fixed-case\"> DJ<\/jats:styled-content>\u20101 translocated into the healthy mitochondria, and significant levels of <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 protein were detected. Treatment with anti\u2010<jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 antibody reduced cell viability and mitochondrial activity, and increased glutathione level. Interestingly, <jats:styled-content style=\"fixed-case\">OGD<\/jats:styled-content> reversed the ratio of astrocyte\/neuron cells (6\/4 to 4\/6).<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>Altogether, these results revealed that <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 participates in the acute endogenous neuroprotection after stroke via the mitochondrial pathway. That <jats:styled-content style=\"fixed-case\">DJ<\/jats:styled-content>\u20101 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.<\/jats:p><\/jats:sec>","DOI":"10.1111\/cns.12208","type":"journal-article","created":{"date-parts":[[2013,12,30]],"date-time":"2013-12-30T10:50:49Z","timestamp":1388400649000},"page":"275-281","source":"Crossref","is-referenced-by-count":34,"title":["Oxygen\u2013Glucose\u2010Deprived Rat Primary Neural Cells Exhibit <scp>DJ<\/scp>\u20101 Translocation into Healthy Mitochondria: A Potent Stroke Therapeutic Target"],"prefix":"10.1111","volume":"20","author":[{"given":"Yuji","family":"Kaneko","sequence":"first","affiliation":[{"name":"Department of Neurosurgery and Brain Repair University of South Florida Morsani College of Medicine Tampa FL 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