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Sci Rep. 2016 Aug 26;6:31373. doi: 10.1038/srep31373.

The Cytomegalovirus protein pUL37×1 targets mitochondria to mediate neuroprotection.

Author information

1
Department of Clinical Neuroscience, UCL Institute of Neurology, University College London, UK.
2
Department of Neurology, Shuang Ho Hospital, Taipei Medical University, New Taipei City, Taiwan.
3
Department of Neurology, School of Medicine, College of Medicine, Taipei Medical University, Taipei, Taiwan.

Abstract

There is substantial evidence that mitochondrial dysfunction plays a significant role in the pathogenesis of Parkinson disease (PD). This contribution probably encompasses defects of oxidative phosphorylation, mitochondrial turnover (mitophagy), mitochondrial derived oxidative stress, and apoptotic signalling. Human cytomegalovirus immediate-early protein pUL37 × 1 induces Bax mitochondrial translocation and inactivation to prevent apoptosis. Over-expressing pUL37 × 1 in neuronal cells protects against staurosporin and 6-hydroxydopamine induced apoptosis and cell death. Protection is not enhanced by bax silencing in pUL37 × 1 over-expressing cells, suggesting a bax-dependent mechanism of action. pUL37 × 1 increases glycolysis and induces mitochondrial hyperpolarization, a bax independent anti-apoptotic action. pUL37 × 1 increases glycolysis through activation of phosphofructokinase by a calcium-dependent pathway. The dual anti-apoptotic mechanism of pUL37 × 1 may be considered a novel neuroprotective strategy in diseases where mitochondrial dysfunction and apoptotic pathways are involved.

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