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The Journal of Neuroscience, December 13, 2006, 26(50):12896-12903; doi:10.1523/JNEUROSCI.3670-06.2006

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Neurobiology of Disease
Bim and Noxa Are Candidates to Mediate the Deleterious Effect of the NF-B Subunit RelA in Cerebral Ischemia

Ioana Inta,¹ Stephan Paxian,² Ira Maegele,¹ Wen Zhang,¹ Marina Pizzi,³ PierFranco Spano,³ Ilenia Sarnico,³ Sajjad Muhammad,¹ Oliver Herrmann,¹ Dragos Inta,¹ Bernd Baumann,⁴ Hsiou-Chi Liou,⁵ Roland M. Schmid,⁶ and Markus Schwaninger¹

¹Department of Neurology, University of Heidelberg, 69120 Heidelberg, Germany, ²Molecular Neurology Unit, Department of Neurology, University of Muenster, 48129 Muenster, Germany, ³Division of Pharmacology and Experimental Therapeutics, Department of Biomedical Sciences and Biotechnologies, School of Medicine, University of Brescia, 25123 Brescia, Italy, ⁴Department of Physiological Chemistry, University of Ulm, 89081 Ulm, Germany, ⁵Department of Medicine, Division of Immunology, Weill Medical College of Cornell University, New York, New York 10021, and ⁶Department of Internal Medicine II, Technical University of Munich, 81675 Munich, Germany

Correspondence should be addressed to Markus Schwaninger, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120 Heidelberg, Germany. Email: markus.schwaninger{at}med.uni-heidelberg.de

The transcription factor nuclear factor B (NF-B) is well known for its antiapoptotic action. However, in some disorders, such as cerebral ischemia, a proapoptotic function of NF-B has been demonstrated. To analyze which subunit of NF-B is functional in cerebral ischemia, we induced focal cerebral ischemia in mice with a germline deletion of the p52 or c-Rel gene or with a conditional deletion of RelA in the brain. Only RelA deficiency reduced infarct size. Interestingly, expression of the proapoptotic BH3 (Bcl-2 homology domain 3)-only genes Bim and Noxa in cerebral ischemia depended on RelA and the upstream kinase IKK (IB kinase). RelA stimulated Bim and Noxa gene transcription in primary cortical neurons and bound to the promoter of both genes. Thus, the deleterious function in cerebral ischemia is specific for the NF-B subunit RelA and may be mediated through Bim and Noxa.

Key words: Bim; Noxa; cerebral ischemia; RelA; c-Rel; p52

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Received Feb. 13, 2006; revised Oct. 4, 2006; accepted Oct. 4, 2006.

Correspondence should be addressed to Markus Schwaninger, Department of Neurology, University of Heidelberg, Im Neuenheimer Feld 400, 69120 Heidelberg, Germany. Email: markus.schwaninger{at}med.uni-heidelberg.de

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