Uncoupling protein-2 prevents neuronal death and diminishes brain dysfunction after stroke and brain trauma View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2003-08

AUTHORS

Gustav Mattiasson, Mehrdad Shamloo, Gunilla Gido, Kavitha Mathi, Gregor Tomasevic, Saili Yi, Craig H. Warden, Roger F. Castilho, Thorsten Melcher, Mirella Gonzalez-Zulueta, Karoly Nikolich, Tadeusz Wieloch

ABSTRACT

Whereas uncoupling protein 1 (UCP-1) is clearly involved in thermogenesis, the role of UCP-2 is less clear. Using hybridization, cloning techniques and cDNA array analysis to identify inducible neuroprotective genes, we found that neuronal survival correlates with increased expression of Ucp2. In mice overexpressing human UCP-2, brain damage was diminished after experimental stroke and traumatic brain injury, and neurological recovery was enhanced. In cultured cortical neurons, UCP-2 reduced cell death and inhibited caspase-3 activation induced by oxygen and glucose deprivation. Mild mitochondrial uncoupling by 2,4-dinitrophenol (DNP) reduced neuronal death, and UCP-2 activity was enhanced by palmitic acid in isolated mitochondria. Also in isolated mitochondria, UCP-2 shifted the release of reactive oxygen species from the mitochondrial matrix to the extramitochondrial space. We propose that UCP-2 is an inducible protein that is neuroprotective by activating cellular redox signaling or by inducing mild mitochondrial uncoupling that prevents the release of apoptogenic proteins. More... »

PAGES

1062-1068

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/nm903

DOI

http://dx.doi.org/10.1038/nm903

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1011171935

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/12858170


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