Mehrabian Zara, Chandrasekaran Krish, Kalakonda Sudhakar, Kristian Tibor, Fiskum Gary, Kalvakolanu Dhananjaya V
Department of Anesthesiology, University of Maryland School of Medicine, 685 W. Baltimore Street, Baltimore, MD 21201, USA.
J Interferon Cytokine Res. 2007 May;27(5):383-92. doi: 10.1089/jir.2006.0067.
The induction of GRIM-19 has been shown to be essential for interferon-beta (IFN-beta)-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 approximately 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.
GRIM-19的诱导已被证明对于干扰素-β（IFN-β）诱导和视黄酸（RA）诱导的肿瘤细胞死亡至关重要。我们研究了GRIM-19在神经细胞中IFN/RA诱导的细胞死亡以及局灶性脑缺血中的定位和水平。暴露于IFN/RA导致人神经母细胞瘤SH-SY5Y细胞中GRIM-19蛋白水平增加约15倍，并诱导超过50%的细胞死亡。在永久性局灶性脑缺血的大鼠中，与对侧（未受影响）半球相比，同侧（受影响）半球的氧化应激增加，GRIM mRNA水平增加（32倍），GRIM-19蛋白水平增加（超过50%）。这些结果表明GRIM-19可能在缺血诱导的神经元细胞死亡中起作用。
