DJ-1 ameliorates ischemic cell death in vitro possibly via mitochondrial pathway

作者：Kaneko Yuji; Shojo Hideki; Burns Jack; Staples Meaghan; Tajiri Naoki; Borlongan Cesar V^*

来源：Neurobiology of Disease, 2014, 62: 56-61.

DOI：10.1016/j.nbd.2013.09.007

• Stroke
• Mitochondria
• Stem cells
• Cell death
• Neuroprotection

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.

• 出版日期2014-2