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- Title
Fas/CD95 Regulatory Protein Faim2 Is Neuroprotective after Transient Brain Ischemia.
- Authors
Reich, Arno; Spering, Christopher; Gertz, Karen; Harms, Christoph; Gerhardt, Ellen; Kronenberg, Golo; Nave, Klaus A.; Schwab, Markus; Tauber, Simone C.; Drinkut, Anja; Harms, Kristian; Beier, Chrstioph P.; Voigt, Aaron; Göbbels, Sandra; Endres, Matthias; Schulz, Jörg B.
- Abstract
Death receptor (DR) signaling has a major impact on the outcome of numerous neurological diseases, including ischemic stroke. DRs mediate not only cell death signals, but also proinflammatory responses and cell proliferation. Identification of regulatory proteins that control the switch between apoptotic and alternative DR signaling opens new therapeutic opportunities. Fas apoptotic inhibitory molecule 2 (Faim2) is an evolutionary conserved, neuron-specific inhibitor of Fas/CD95-mediated apoptosis. To investigate its role during development and in disease models, we generated Faim2-deficient mice. The ubiquitous null mutation displayed a viable and fertile phenotype without overt deficiencies. However, lack of Faim2 caused an increase in susceptibility to combined oxygen- glucose deprivation in primary neurons in vitro as well as in caspase-associated cell death, stroke volume, and neurological impairment after cerebral ischemia in vivo. These processes were rescued by lentiviral Faim2 gene transfer. In summary, we provide evidence that Faim2 is a novel neuroprotective molecule in the context of cerebral ischemia.
- Subjects
NEUROPROTECTIVE agents; ISCHEMIA; DEATH receptors; LABORATORY mice; CELL death; PHENOTYPES
- Publication
Journal of Neuroscience, 2011, Vol 31, Issue 1, p225
- ISSN
0270-6474
- Publication type
Article
- DOI
10.1523/JNEUROSCI.2188-10.2011