NF-κB is activated and promotes cell death in focal, cerebral ischemia

Armin Schneider; Ana Martin-Villalba; Falk Weih; Johannes Vogel; Thomas Wirth; Markus Schwaninger

doi:10.1038/8432

NF-κB is activated and promotes cell death in focal, cerebral ischemia

Armin Schneider, Ana Martin-Villalba, Falk Weih, Johannes Vogel, Thomas Wirth, Markus Schwaninger^*

^*Corresponding author for this work

Institute of Experimental and Clinical Pharmacology and Toxicology

616 Citations (Scopus)

Abstract

The transcription factor NF-κB is a regulator of cell death or survival. To investigate the role of NF-κB in neuronal cell death, we studied its activation in a rodent model of stroke. In the ischemic hemisphere, NF-κB was activated, as determined by increased expression of an NF-κB-driven reporter transgene, nuclear translocation of NF-κB in neurons and enhanced DNA binding of NF-κB subunits RelA and p50. In p50 knockout mice, ischemic damage was significantly reduced. This indicates a cell death- promoting role of NF-κB in focal ischemia. NF-κB may provide a new pharmacological target in neurologic disease.

Original language	English
Journal	Nature Medicine
Volume	5
Issue number	5
Pages (from-to)	554-559
Number of pages	6
ISSN	1078-8956
DOIs	https://doi.org/10.1038/8432
Publication status	Published - 01.05.1999

Funding

Acknowledgment We thank P. Chan for help with establishing the filament model in mice; and S. Prinz, N. Attigah, and Y. Xu for their help at various stages of the project. This work was supported by a grant of the DFG to M.S.

Research Areas and Centers

Academic Focus: Center for Brain, Behavior and Metabolism (CBBM)

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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abstract = "The transcription factor NF-κB is a regulator of cell death or survival. To investigate the role of NF-κB in neuronal cell death, we studied its activation in a rodent model of stroke. In the ischemic hemisphere, NF-κB was activated, as determined by increased expression of an NF-κB-driven reporter transgene, nuclear translocation of NF-κB in neurons and enhanced DNA binding of NF-κB subunits RelA and p50. In p50 knockout mice, ischemic damage was significantly reduced. This indicates a cell death- promoting role of NF-κB in focal ischemia. NF-κB may provide a new pharmacological target in neurologic disease.",

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AU - Schwaninger, Markus

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AB - The transcription factor NF-κB is a regulator of cell death or survival. To investigate the role of NF-κB in neuronal cell death, we studied its activation in a rodent model of stroke. In the ischemic hemisphere, NF-κB was activated, as determined by increased expression of an NF-κB-driven reporter transgene, nuclear translocation of NF-κB in neurons and enhanced DNA binding of NF-κB subunits RelA and p50. In p50 knockout mice, ischemic damage was significantly reduced. This indicates a cell death- promoting role of NF-κB in focal ischemia. NF-κB may provide a new pharmacological target in neurologic disease.

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NF-κB is activated and promotes cell death in focal, cerebral ischemia

Abstract

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