在局灶性脑缺血期间，干扰素-β和视黄酸诱导的细胞死亡调节因子GRIM-19表达上调。
The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia.
作者信息
Mehrabian Zara, Chandrasekaran Krish, Kalakonda Sudhakar, Kristian Tibor, Fiskum Gary, Kalvakolanu Dhananjaya V
机构信息
Department of Anesthesiology, University of Maryland School of Medicine, 685 W. Baltimore Street, Baltimore, MD 21201, USA.
出版信息
J Interferon Cytokine Res. 2007 May;27(5):383-92. doi: 10.1089/jir.2006.0067.
Abstract
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.
摘要
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。
相似文献
1
The IFN-beta and retinoic acid-induced cell death regulator GRIM-19 is upregulated during focal cerebral ischemia.在局灶性脑缺血期间，干扰素-β和视黄酸诱导的细胞死亡调节因子GRIM-19表达上调。
J Interferon Cytokine Res. 2007 May;27(5):383-92. doi: 10.1089/jir.2006.0067.
2
Curcumin synergistically increases effects of β-interferon and retinoic acid on breast cancer cells in vitro and in vivo by up-regulation of GRIM-19 through STAT3-dependent and STAT3-independent pathways.姜黄素通过STAT3依赖性和非依赖性途径上调GRIM-19，在体外和体内协同增强β-干扰素和视黄酸对乳腺癌细胞的作用。
J Drug Target. 2017 Mar;25(3):247-254. doi: 10.1080/1061186X.2016.1242132. Epub 2016 Oct 16.
3
Characterization of monoclonal antibodies against GRIM-19, a novel IFN-beta and retinoic acid-activated regulator of cell death.针对GRIM-19的单克隆抗体的特性研究，GRIM-19是一种新型的干扰素-β和视黄酸激活的细胞死亡调节因子。
J Interferon Cytokine Res. 2002 Oct;22(10):1017-26. doi: 10.1089/107999002760624242.
4
GRIM-19 associates with the serine protease HtrA2 for promoting cell death.GRIM-19与丝氨酸蛋白酶HtrA2结合以促进细胞死亡。
Oncogene. 2007 Jul 19;26(33):4842-9. doi: 10.1038/sj.onc.1210287. Epub 2007 Feb 12.
5
Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-beta and retinoic acid-induced cancer cell death.将线粒体呼吸链与细胞死亡相耦合：线粒体复合物I在干扰素-β和视黄酸诱导的癌细胞死亡中的重要作用。
Cell Death Differ. 2007 Feb;14(2):327-37. doi: 10.1038/sj.cdd.4402004. Epub 2006 Jul 7.
6
Identification of GRIM-19, a novel cell death-regulatory gene induced by the interferon-beta and retinoic acid combination, using a genetic approach.利用遗传学方法鉴定GRIM-19，一种由β-干扰素和视黄酸联合诱导的新型细胞死亡调控基因。
J Biol Chem. 2000 Oct 27;275(43):33416-26. doi: 10.1074/jbc.M003929200.
7
The cell death regulator GRIM-19 is an inhibitor of signal transducer and activator of transcription 3.细胞死亡调节因子GRIM-19是信号转导和转录激活因子3的抑制剂。
Proc Natl Acad Sci U S A. 2003 Aug 5;100(16):9342-7. doi: 10.1073/pnas.1633516100. Epub 2003 Jul 16.
8
[Interferon-β combined with all-trans retinoic acid supresses proliferation and promote apoptosis by inhibiting JAK2/STAT3 pathway in HepG2 human hepatocellular carcinoma cells].干扰素-β联合全反式维甲酸通过抑制HepG2人肝癌细胞中的JAK2/STAT3通路抑制增殖并促进凋亡
Xi Bao Yu Fen Zi Mian Yi Xue Za Zhi. 2016 Jul;32(7):901-5.
9
Involvement of GRIM-19 in apoptosis induced in H5N1 virus-infected human macrophages.GRIM-19 在 H5N1 病毒感染的人巨噬细胞中诱导凋亡的作用。
Innate Immun. 2013 Dec;19(6):655-62. doi: 10.1177/1753425913479149. Epub 2013 Mar 25.
10
Identification and characterization of GRIM-1, a cell-death-associated gene product.鉴定和表征细胞死亡相关基因产物 GRIM-19。
J Cell Sci. 2010 Aug 15;123(Pt 16):2781-91. doi: 10.1242/jcs.070250. Epub 2010 Jul 27.
引用本文的文献
1
Targeting STAT3 signaling pathway by curcumin and its analogues for breast cancer: A narrative review.姜黄素及其类似物靶向STAT3信号通路治疗乳腺癌：一项叙述性综述。
Animal Model Exp Med. 2024 Dec;7(6):853-867. doi: 10.1002/ame2.12491. Epub 2024 Sep 2.
2
Heterogeneity of GRIM-19 Expression in the Adult Mouse Brain.成年小鼠大脑中 GRIM-19 表达的异质性。
Cell Mol Neurobiol. 2019 Oct;39(7):935-951. doi: 10.1007/s10571-019-00689-1. Epub 2019 May 21.
3
GRIM-19: A master regulator of cytokine induced tumor suppression, metastasis and energy metabolism.GRIM-19：细胞因子诱导的肿瘤抑制、转移和能量代谢的主要调节因子。
Cytokine Growth Factor Rev. 2017 Feb;33:1-18. doi: 10.1016/j.cytogfr.2016.09.001. Epub 2016 Sep 15.
4
The Effect of Aging on Mitochondrial Complex I and the Extent of Oxidative Stress in the Rat Brain Cortex.衰老对大鼠大脑皮质线粒体复合体I及氧化应激程度的影响。
Neurochem Res. 2016 Aug;41(8):2160-72. doi: 10.1007/s11064-016-1931-z. Epub 2016 May 9.
5
Interferons, signal transduction pathways, and the central nervous system.干扰素、信号转导通路与中枢神经系统。
J Interferon Cytokine Res. 2014 Aug;34(8):559-76. doi: 10.1089/jir.2014.0021.
6
Ischemia-induced inhibition of mitochondrial complex I in rat brain: effect of permeabilization method and electron acceptor.缺血诱导的大鼠脑线粒体复合物 I 抑制：通透化方法和电子受体的影响。
Neurochem Res. 2012 May;37(5):965-76. doi: 10.1007/s11064-011-0689-6. Epub 2012 Jan 5.
7
GRIM-19: A Double-edged Sword that Regulates Anti-Tumor and Innate Immune Responses.GRIM-19：一把调控抗肿瘤和固有免疫反应的双刃剑。
Transl Oncogenomics. 2008 Mar 17;3:67-79.
8
Cytokine-induced tumor suppressors: a GRIM story.细胞因子诱导的肿瘤抑制因子：GRIM 的故事。
Cytokine. 2010 Oct-Nov;52(1-2):128-42. doi: 10.1016/j.cyto.2010.03.009. Epub 2010 Apr 10.
本文引用的文献
1
Coupling mitochondrial respiratory chain to cell death: an essential role of mitochondrial complex I in the interferon-beta and retinoic acid-induced cancer cell death.将线粒体呼吸链与细胞死亡相耦合：线粒体复合物I在干扰素-β和视黄酸诱导的癌细胞死亡中的重要作用。
Cell Death Differ. 2007 Feb;14(2):327-37. doi: 10.1038/sj.cdd.4402004. Epub 2006 Jul 7.
2
Isolation of mitochondria with high respiratory control from primary cultures of neurons and astrocytes using nitrogen cavitation.利用氮气空化从神经元和星形胶质细胞原代培养物中分离具有高呼吸控制率的线粒体。
J Neurosci Methods. 2006 Apr 15;152(1-2):136-43. doi: 10.1016/j.jneumeth.2005.08.018. Epub 2005 Oct 25.
3
Point mutation in GRIM-19: a new genetic lesion in Hurthle cell thyroid carcinomas.GRIM-19中的点突变：甲状腺嗜酸性细胞癌中的一种新的基因损伤。
Br J Cancer. 2005 May 23;92(10):1817-8. doi: 10.1038/sj.bjc.6602556.
4
Regulation of mitochondrial gene expression by energy demand in neural cells.神经细胞中能量需求对线粒体基因表达的调控。
J Neurochem. 2005 May;93(4):850-60. doi: 10.1111/j.1471-4159.2005.03066.x.
5
Somatic and germline mutation in GRIM-19, a dual function gene involved in mitochondrial metabolism and cell death, is linked to mitochondrion-rich (Hurthle cell) tumours of the thyroid.GRIM-19是一种参与线粒体代谢和细胞死亡的双功能基因，其体细胞和生殖系突变与富含线粒体的（许特耳细胞）甲状腺肿瘤有关。
Br J Cancer. 2005 May 23;92(10):1892-8. doi: 10.1038/sj.bjc.6602547.
6
Mitochondrial metabolism of reactive oxygen species.活性氧的线粒体代谢
Biochemistry (Mosc). 2005 Feb;70(2):200-14. doi: 10.1007/s10541-005-0102-7.
7
GRIM-19, a cell death regulatory protein, is essential for assembly and function of mitochondrial complex I.GRIM-19是一种细胞死亡调节蛋白，对线粒体复合体I的组装和功能至关重要。
Mol Cell Biol. 2004 Oct;24(19):8447-56. doi: 10.1128/MCB.24.19.8447-8456.2004.
8
Mitochondrial mechanisms of neural cell apoptosis.神经细胞凋亡的线粒体机制
J Neurochem. 2004 Sep;90(6):1281-9. doi: 10.1111/j.1471-4159.2004.02572.x.
9
Acute and persistent protein synthesis inhibition following cerebral reperfusion.
J Neurosci Res. 2004 Sep 15;77(6):771-6. doi: 10.1002/jnr.20225.
10
Mitochondrial calcium and oxidative stress as mediators of ischemic brain injury.线粒体钙和氧化应激作为缺血性脑损伤的介质
Cell Calcium. 2004 Sep-Oct;36(3-4):257-64. doi: 10.1016/j.ceca.2004.02.012.
Zotero 插件