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Journal of Interferon & Cytokine Research
The IFN-β and Retinoic Acid-Induced Cell Death Regulator GRIM-19 is Upregulated During Focal Cerebral Ischemia
To cite this article:
Zara Mehrabian, Krish Chandrasekaran, Sudhakar Kalakonda, Tibor Kristian, Gary Fiskum, Dhananjaya V. Kalvakolanu.
Journal of Interferon & Cytokine Research.
May 2007,
27(5): 383-392.
doi:10.1089/jir.2006.0067.
Zara Mehrabian Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201. Krish Chandrasekaran Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201. Sudhakar Kalakonda Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201. Tibor Kristian Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201. Gary Fiskum Department of Anesthesiology, University of Maryland School of Medicine, Baltimore, MD 21201. Dhananjaya V. Kalvakolanu Department of Microbiology and Immunology, University of Maryland School of Medicine, Baltimore, MD 21201. The induction of GRIM-19 has been shown to be essential for interferon-β (IFN-β)-induced and retinoic acid (RA)-induced tumor cell death. We have studied the localization and levels of GRIM-19 in IFN/RA-induced cell death in neural cells and in focal cerebral ischemia. Exposure to IFN/RA caused a ˜ 15-fold increase in GRIM-19 protein levels and induced >50% cell death in human neuroblastoma SH-SY5Y cells. In rats subjected to permanent focal cerebral ischemia, increased oxidative stress, as well as increased GRIM mRNA levels (32-fold) and increased GRIM-19 (>50%) protein levels were noted in the ipsilateral (affected) hemisphere compared with the contralateral (unaffected) hemisphere. These results suggest that GRIM-19 may play a role in ischemia-induced neuronal cell death.
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