Uncoupling protein 2 in the glial response to stress: Implications for neuroprotection

Daniel T. Hass, Colin J. Barnstable

Research output: Contribution to journalReview articlepeer-review

22 Scopus citations

Abstract

Reactive oxygen species (ROS) are free radicals thought to mediate the neurotoxic effects of several neurodegenerative disorders. In the central nervous system, ROS can also trigger a phenotypic switch in both astrocytes and microglia that further aggravates neurodegeneration, termed reactive gliosis. Negative regulators of ROS, such as mitochondrial uncoupling protein 2 (UCP2) are neuroprotective factors that decrease neuron loss in models of stroke, epilepsy, and parkinsonism. However, it is unclear whether UCP2 acts purely to prevent ROS production, or also to prevent gliosis. In this review article, we discuss published evidence supporting the hypothesis that UCP2 is a neuroprotective factor both through its direct effects in decreasing mitochondrial ROS and through its effects in astrocytes and microglia. A major effect of UCP2 activation in glia is a change in the spectrum of secreted cytokines towards a more anti-inflammatory spectrum. There are multiple mechanisms that can control the level or activity of UCP2, including a variety of metabolites and microRNAs. Understanding these mechanisms will be key to exploitingthe protective effects of UCP2 in therapies for multiple neurodegenerative conditions.

Original languageEnglish (US)
Pages (from-to)1197-1200
Number of pages4
JournalNeural Regeneration Research
Volume11
Issue number8
DOIs
StatePublished - Aug 2016

All Science Journal Classification (ASJC) codes

  • Developmental Neuroscience

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