Journal
JOURNAL OF NEUROSCIENCE
Volume 31, Issue 1, Pages 225-233Publisher
SOC NEUROSCIENCE
DOI: 10.1523/JNEUROSCI.2188-10.2011
Keywords
-
Categories
Funding
- German Research Council (DFG) through the DFG-Research Center for Molecular Physiology of the Brain
- RWTH Aachen University, Faculty of Medicine [AG START, 690945/145/09]
- BMBF (Center for Stroke Research)
- DFG (SFB-TR)
- Volkswagen Foundation
- European Union (ARISE and EUStroke Consortia)
Ask authors/readers for more resources
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.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available