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中华神经创伤外科电子杂志 ›› 2020, Vol. 06 ›› Issue (02) : 113 -117. doi: 10.3877/cma.j.issn.2095-9141.2020.02.011

所属专题: 文献

综述

Small Maf转录因子在神经系统疾病中的作用研究进展
高飞1, 刘佰运2, 茆翔3,()   
  1. 1. 100070 北京,首都医科大学附属北京天坛医院神经外科
    2. 100070 北京市神经外科研究所中枢神经系统损伤研究北京市重点实验室和首都医科大学附属北京天坛医院神经外科
    3. 230022 合肥,安徽医科大学第一附属医院神经外科
  • 收稿日期:2019-12-01 出版日期:2020-04-15
  • 通信作者: 茆翔
  • 基金资助:
    国家自然科学基金(81171144,81471238); 北京市卫生健康委员会2020年预算项目(PXM2020_026280_000002)

Research progress on the role of small Maf transcription factors in neurological diseases

Fei Gao1, Baiyun Liu2, Xiang Mao3,()   

  1. 1. Department of Neurosurgery, Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China
    2. Beijing Key Laboratory of Central Nervous System Injury and Department of Neurosurgery, Beijing Neurosurgical Institute and Beijing Tiantan Hospital, Capital Medical University, Beijing 100070, China
    3. Department of Neurosurgery, the First Affiliated Hospital of Anhui Medical University, Hefei 230022, China
  • Received:2019-12-01 Published:2020-04-15
  • Corresponding author: Xiang Mao
  • About author:
    Corresponding author: Mao Xiang, Email:
引用本文:

高飞, 刘佰运, 茆翔. Small Maf转录因子在神经系统疾病中的作用研究进展[J]. 中华神经创伤外科电子杂志, 2020, 06(02): 113-117.

Fei Gao, Baiyun Liu, Xiang Mao. Research progress on the role of small Maf transcription factors in neurological diseases[J]. Chinese Journal of Neurotraumatic Surgery(Electronic Edition), 2020, 06(02): 113-117.

Small Maf转录因子(sMafs),即MafF、MafG、MafK,一组含有碱性亮氨酸拉链结构的高度同源性蛋白,由于其自身缺乏转录激活域,在体内主要与Cap'n’Collar蛋白及Bach蛋白形成异源二聚体,以及自身之间形成同源二聚体发挥作用。氧化应激和炎症反应是神经系统疾病中的共同特征,并在神经损伤、神经认知、神经发育及其他神经功能中具有损伤性的作用。sMafs在氧化应激和炎症反应中起着保护作用,本文现就sMafs在神经系统疾病中的抗氧化、抗炎以及其在神经损伤、认知、发育及其他的作用机制作一综述。

Small Maf transcription factors (sMafs), including MafF, MafG, and MafK, are a group of highly homologous proteins containing a basic leucine zipper structure. Due to their lack of a transcription activation domain, sMafs mainly interact with Cap'n’Collar and Bach proteins form heterodimers, as well as homodimers between themselves. Oxidative stress and inflammatory response are common features in neurological diseases and have damaging effects on nerve injury, neurocognition, neurodevelopment, and other neural functions. sMafs play a protective role in oxidative stress and inflammatory response. In this paper, the antioxidation and anti-inflammatory effects of sMafs in neurological diseases, as well as their mechanisms of neurological damage, cognition, development and other aspects are reviewed.

[1]
Katsuoka F, Yamamoto M. Small Maf proteins (MafF, MafG, MafK): history, structure and function[J]. Gene, 2016, 586(2): 197-205.
[2]
Toki T, Itoh J, Kitazawa J, et al. Human small Maf proteins form heterodimers with cnc family transcription factors and recognize the NF-E2 motif[J]. Oncogene, 1997, 14(16): 1901-1910.
[3]
Motohashi H, O’Connor T, Katsuoka F, et al. Integration and diversity of the regulatory network composed of Maf and CNC families of transcription factors[J]. Gene, 2002, 294(1-2): 1-12.
[4]
Katsuoka F, Motohashi H, Ishii T, et al. Genetic evidence that small Maf proteins are essential for the activation of antioxidant response element-dependent genes[J]. Mol Cell Biol, 2005, 25(18): 8044-8051.
[5]
Nishizawa M, Kataoka K, Goto N, et al. V-Maf, a viral oncogene that encodes a "leucine zipper" motif[J]. Proc Natl Acad Sci USA, 1989, 86(20): 7711-7715.
[6]
Kannan MB, Solovieva V, Blank V. The small Maf transcription factors MafF, MafG and MafK: current knowledge and perspectives[J]. Biochim Biophys Acta, 2012, 1823(10): 1841-1846.
[7]
Benkhelifa S, Provot S, Lecoq O, et al. MafA, a novel member of the Maf proto-oncogene family, displays developmental regulation and mitogenic capacity in avian neuroretina cells[J]. Oncogene, 1998, 17(2): 247-254.
[8]
Massrieh W, Derjuga A, Doualla-Bell F, et al. Regulation of the MafF transcription factor by proinflammatory cytokines in myometrial cells[J]. Biol Reprod, 2006, 74(4): 699-705.
[9]
Carvajal-Yepes M, Himmelsbach K, Schaedler S, et al. Hepatitis C virus impairs the induction of cytoprotective Nrf2 target genes by delocalization of small Maf proteins[J]. J Biol Chem, 2011, 286(11): 8941-8951.
[10]
Kusunoki H, Motohashi H, Katsuoka F, et al. Solution structure of the DNA-binding domain of MafG[J]. Nat Struct Biol, 2002, 9(4): 252-256.
[11]
Kerppola TK, Curran T. Maf and Nrl can bind to AP-1 sites and form heterodimers with Fos and Jun[J]. Oncogene, 1994, 9(3): 675-684.
[12]
Kimura M, Yamamoto T, Zhang J, et al. Molecular basis distinguishing the DNA binding profile of Nrf2-Maf heterodimer from that of Maf homodimer[J]. J Biol Chem, 2015, 290(17): 10644.
[13]
Igarashi K, Kataoka K, Itoh K, et al. Regulation of transcription by dimerization of erythroid factor NF-E2 p45 with small Maf proteins[J]. Nature, 1994, 367(6463): 568-572.
[14]
Blank V. Small Maf proteins in mammalian gene control: Mere dimerization partners or dynamic transcriptional regulators?[J]. J Mol Biol, 2008, 376(4): 913-925.
[15]
Dhakshinamoorthy S, Jaiswal AK. Small Maf (MafG and MafK) proteins negatively regulate antioxidant response element-mediated expression and antioxidant induction of the NAD(P)H: Quinone oxidoreductase1 gene[J]. J Biol Chem, 2000, 275(51): 40134-40141.
[16]
Nguyen T, Huang HC, Pickett CB. Transcriptional regulation of the antioxidant response element. Activation by Nrf2 and repression by MafK[J]. J Biol Chem, 2000, 275(20): 15466-15473.
[17]
Amit I, Citri A, Shay T, et al. A module of negative feedback regulators defines growth factor signaling[J]. Nat Genet, 2007, 39(4): 503-512.
[18]
Katsuoka F, Yamazaki H, Yamamoto M. Small Maf deficiency recapitulates the liver phenotypes of nrf1- and Nrf2-deficient mice[J]. Genes Cells, 2016, 21(12): 1309-1319.
[19]
Islam MT. Oxidative stress and mitochondrial dysfunction-linked neurodegenerative disorders[J]. Neurol Res, 2017, 39(1): 73-82.
[20]
Salim S. Oxidative stress and the central nervous system[J]. J Pharmacol Exp Ther, 2017, 360(1): 201-205.
[21]
Ferrero-Miliani L, Nielsen OH, Andersen PS, et al. Chronic inflammation: Importance of NOD2 and NALP3 in interleukin-1beta generation[J]. Clin Exp Immunol, 2007, 147(2): 227-235.
[22]
Khansari N, Shakiba Y, Mahmoudi M. Chronic inflammation and oxidative stress as a major cause of age-related diseases and cancer[J]. Recent Pat Inflamm Allergy Drug Discov, 2009, 3(1): 73-80.
[23]
Ahmed SM, Luo L, Namani A, et al. Nrf2 signaling pathway: Pivotal roles in inflammation[J]. Biochim Biophys Acta Mol Basis Dis, 2017, 1863(2): 585-597.
[24]
Morin P, Jr., Ni Z, McMullen DC, et al. Expression of Nrf2 and its downstream gene targets in hibernating 13-lined ground squirrels, spermophilus tridecemlineatus[J]. Mol Cell Biochem, 2008, 312(1-2): 121-129.
[25]
Ni Z, Storey KB. Heme oxygenase expression and Nrf2 signaling during hibernation in ground squirrels[J]. Can J Physiol Pharmacol, 2010, 88(3): 379-387.
[26]
Kosuru R, Kandula V, Rai U, et al. Pterostilbene decreases cardiac oxidative stress and inflammation via activation of AMPK/Nrf2/HO-1 pathway in fructose-fed diabetic rats[J]. Cardiovasc Drugs Ther, 2018, 32(2): 147-163.
[27]
Li W, Yu S, Liu T, et al. Heterodimerization with small Maf proteins enhances nuclear retention of Nrf2 via masking the neszip motif[J]. Biochim Biophys Acta, 2008, 1783(10): 1847-1856.
[28]
Chen XL, Dodd G, Thomas S, et al. Activation of Nrf2/are pathway protects endothelial cells from oxidant injury and inhibits inflammatory gene expression[J]. Am J Physiol Heart Circ Physiol, 2006, 290(5): H1862-H1870.
[29]
Braun S, Hanselmann C, Gassmann MG, et al. Nrf2 transcription factor, a novel target of keratinocyte growth factor action which regulates gene expression and inflammation in the healing skin wound[J]. Mol Cell Biol, 2002, 22(15): 5492-5505.
[30]
Arisawa T, Tahara T, Shibata T, et al. The relationship between helicobacter pylori infection and promoter polymorphism of the Nrf2 gene in chronic gastritis[J]. Int J Mol Med, 2007, 19(1): 143-148.
[31]
Shavit JA, Motohashi H, Onodera K, et al. Impaired megakaryopoiesis and behavioral defects in MafG-null mutant mice[J]. Genes Dev, 1998, 12(14): 2164-2174.
[32]
Katsuoka F, Motohashi H, Tamagawa Y, et al. Small Maf compound mutants display central nervous system neuronal degeneration, aberrant transcription, and bach protein mislocalization coincident with myoclonus and abnormal startle response[J]. Mol Cell Biol, 2003, 23(4): 1163-1174.
[33]
Lee CS, Lee C, Hu T, et al. Loss of nuclear factor E2-related factor 1 in the brain leads to dysregulation of proteasome gene expression and neurodegeneration[J]. Proc Natl Acad Sci USA, 2011, 108(20): 8408-8413.
[34]
Wood RL, Rutterford NA. Demographic and cognitive predictors of long-term psychosocial outcome following traumatic brain injury[J]. J Int Neuropsychol Soc, 2006, 12(3): 350-358.
[35]
Zhou C, Guan XJ, Guo T, et al. Progressive brain atrophy in parkinson’s disease patients who convert to mild cognitive impairment[J]. CNS Neurosci Ther, 2020, 26(1): 117-125.
[36]
Oertel FC, Schliesseit J, Brandt AU, et al. Cognitive impairment in neuromyelitis optica spectrum disorders: a review of clinical and neuroradiological features[J]. Front Neurol, 2019, 10: 608.
[37]
Ghirnikar RS, Lee YL, Eng LF. Inflammation in traumatic brain injury: role of cytokines and chemokines[J]. Neurochem Res, 1998, 23(3): 329-340.
[38]
Cook AL, Vitale AM, Ravishankar S, et al. Nrf2 activation restores disease related metabolic deficiencies in olfactory neurosphere-derived cells from patients with sporadic parkinson’s disease[J]. PLoS One, 2011, 6(7): e21907.
[39]
Lu XY, Wang HD, Xu JG, et al. Pretreatment with tert-butylhydroquinone attenuates cerebral oxidative stress in mice after traumatic brain injury[J]. J Surg Res, 2014, 188(1): 206-212.
[40]
Jin W, Wang H, Yan W, et al. Role of Nrf2 in protection against traumatic brain injury in mice[J]. J Neurotrauma, 2009, 26(1): 131-139.
[41]
Itoh K, Chiba T, Takahashi S, et al. An Nrf2/small Maf heterodimer mediates the induction of phase II detoxifying enzyme genes through antioxidant response elements[J]. Biochem Biophys Res Commun, 1997, 236(2): 313-322.
[42]
Ding H, Wang H, Zhu L, et al. Ursolic acid ameliorates early brain injury after experimental traumatic brain injury in mice by activating the Nrf2 pathway[J]. Neurochem Res, 2017, 42(2): 337-346.
[43]
Wang Q, Li WX, Dai SX, et al. Meta-analysis of parkinson's disease and alzheimer’s disease impaired pathways and dysregulation of Nrf2-dependent genes[J]. J Alzheimers Dis, 2017, 56(4): 1525-1539.
[44]
Huang M, Zeng S, Zou Y, et al. The suppression of bromodomain and extra-terminal domain inhibits vascular inflammation by blocking NF-kappaB and MAPK activation[J]. Br J Pharmacol, 2017, 174(1): 101-115.
[45]
Rangasamy T, Guo J, Mitzner WA, et al. Disruption of Nrf2 enhances susceptibility to severe airway inflammation and asthma in mice[J]. J Exp Med, 2005, 202(1): 47-59.
[46]
Osburn WO, Karim B, Dolan PM, et al. Increased colonic inflammatory injury and formation of aberrant crypt foci in Nrf2-deficient mice upon dextran sulfate treatment[J]. Int J Cancer, 2007, 121(9): 1883-1891.
[47]
Lee DS, Jeong GS. Arylbenzofuran isolated from dalbergia odorifera suppresses lipopolysaccharide-induced mouse BV2 microglial cell activation, which protects mouse hippocampal HT22 cells death from neuroinflammation-mediated toxicity[J]. Eur J Pharmacol, 2014, 728: 1-8.
[48]
Ro YT, Jang BK, Shin CY, et al. Akt regulates the expression of MafK, synaptotagmin I, and syntenin-1, which play roles in neuronal function[J]. J Biomed Sci, 2010, 17(1): 18.
[49]
Dijkmans TF, van Hooidonk LWA, Schouten TG, et al. Identification of new nerve growth factor-responsive immediate-early genes[J]. Brain Res, 2009, 1249: 19-33.
[50]
Dong W, Yang B, Wang L, et al. Curcumin plays neuroprotective roles against traumatic brain injury partly via Nrf2 signaling[J]. Toxicol Appl Pharmacol, 2018, 346: 28-36.
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