硒蛋白在阿尔茨海默病的作用研究进展
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摘要
阿尔茨海默病(Alzheimer's disease, AD)是一种中枢神经系统的退行性疾病,在老年人群中极为常见,其防治问题是世界难题之一。硒蛋白(selenoprotein)是微量元素硒在人体和动物体内存在和发挥生物功能的主要形式。近年来,研究硒及硒蛋白与阿尔茨海默病关系的文章逐渐增多,表明硒及硒蛋白对阿尔茨海默病有明显的防治作用,这为阿尔茨海默病防治提供了新的思路。现对硒蛋白在阿尔茨海默病的发生及发展方面的作用进行系统总结,为阿尔茨海默病的预防与治疗提供新的思路。
Alzheimer's disease(AD) is a neurodegenerative disease that is extremely common in the aged and its prevention and treatment is one of the world's problems. Selenoproteins are the main form of microelement selenium that exists in the body of humen and animals and exerting its biological functions. In recent years, more and more articles focused on the role of selenium and selenoproteins, providing a new idea for the prevention and treatment of AD. This paper systematically summarizes the researches of selenoproteins on the occurrence and development of AD and provides a new idea for the prevention and treatment of the disease.
Alzheimer's disease(AD) is a neurodegenerative disease that is extremely common in the aged and its prevention and treatment is one of the world's problems. Selenoproteins are the main form of microelement selenium that exists in the body of humen and animals and exerting its biological functions. In recent years, more and more articles focused on the role of selenium and selenoproteins, providing a new idea for the prevention and treatment of AD. This paper systematically summarizes the researches of selenoproteins on the occurrence and development of AD and provides a new idea for the prevention and treatment of the disease.
引文
[1]Folch J,Petrov D,Ettcheto M,et al.Current research therapeutic strategies for Alzheimer's disease treatment.Neural Plast,2016,2016:8501693
[2]赵娟.BACE基因在阿尔兹海默症中作用机制的研究[D].北京:北京理工大学,2008
[3]Hort J,O'Brien JT,Gainotti G,et al.EFNS guidelines for the diagnosis and management of Alzheimer's disease.Eur J Neurol,2010,17:1236-48
[4]赵丽波,付宏娟,张健莉.阿尔茨海默病发生机制的研究进展.中国老年学,2011,31:4997-8
[5]马云峰,王湘庆,郎森阳.微管相关蛋白Tau蛋白及Tau病的研究进展.解放军医学院学报,2015,36:621-4
[6]王玲,朱鸣峰.阿尔茨海默病发病机制的研究进展.吉林医学,2013,34:531-2
[7]Sakono M,Zako T.Amyloid oligomers:formation and toxicity of Aβoligomers.FEBS J,2010,277:1348-58
[8]Cardoso BR,Roberts BR,Bush AI,et al.Selenium,selenoproteins and neurodegenerative diseases.Metallomics,2015,7:1213-28
[9]Cheignon C,Tomas M,Bonnefont-Rousselot D,et al.Oxidative stress and the amyloidβpeptide in Alzheimer's disease.Redox Biol,2018,14:450-64
[10]Nesi G,Sestito S,Digiacomo M,et al.Oxidative stress,mitochondrial abnormalities and proteins deposition:multitarget approaches in Alzheimer's disease.Curr Top Med Chem,2017,17:3062-79
[11]刘晓杰,杨威,祁金顺.氧化应激与阿尔茨海默病.生理学报,2012,64:87-95
[12]Steffen J,Krohn M,Schwitlick C,et al.Expression of endogenous mouse APP modulatesβ-amyloid deposition in hAPP-transgenic mice.Acta Neuropathol Commun,2017,5:49
[13]Sastre M,Walter J,Gentleman SM.Interactions between APP secretases and inflammatory mediators.J Neuroinflamm,2008,5:1-11
[14]Marco LY,Venneri A,Farkas E,et al.Vascular dysfunction in the pathogenesis of Alzheimer's disease-A review of endothelium-mediated mechanisms and ensuing vicious circles.Neurobiol Dis,2015,82:593-606
[15]Mcinerney MP,Short JL,Nicolazzo JA.Neurovascular alterations in Alzheimer’s disease:transporter expression profiles and CNS drug access.AAPS J,2017,19:940-56
[16]Kivipelto M,Nqandu T,Fratiqlioni L,et al.Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease.Arch Neurol,2005,62:1556-60
[17]Hokama M,Oka S,Leon J,et al.Altered expression of diabetes-related genes in Alzheimer’s disease brains:the Hisayama study.Cereb Cortex,2014,24:2476-88
[18]Li J,Liu D,Sun L,et al.Advanced glycation end products and neurodegenerative diseases:mechanisms and perspective.J Neurol Sci,2012,317:1-5
[19]陈长兰,郇丰宁,孟雪莲.硒对人体的作用机理及科学补硒方法.辽宁大学学报(自然科学版),2016,43:155-68
[20]Dominiak A,Wilkaniec A,J??ko H,et al.Selol,an organic selenium donor,prevents lipopolysaccharide-induced oxidative stress and inflammatory reaction in the rat brain.Neurochem Int,2017,108:66-77
[21]Aaseth J,Alexander J,Bj?rklund G,et al.Treatment strategies in Alzheimer's disease:a review with focus on selenium supplementation.Biometals,2016,29:827-39
[22]Nakayama A,Hill KE,Austin LM,et al.All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium.Eur J Nutr,2007,137:690-3
[23]Schweizer U,Streckfuss F,Pelt P,et al.Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply.Biochem J,2005,386:221-6
[24]Rita CB,Silva BV,Jacob FW,et al.Selenium status in elderly:relation to cognitive decline.J Trace Elem Med Biol,2014,28:422-6
[25]Olde Rikkert MG,Verhey FR,Sijben JW,et al.Differences in nutritional status between very mild Alzheimer's disease patients and healthy controls.J Alzheimers Dis,2014,41:261-71
[26]Kryukov GV,Castellano S,Novoselov SV,et al.Characterization of mammalian selenoproteomes.Science,2003,300:1439-43
[27]Dery L,Reddy PS,Dery S,et al.Accessing human selenoproteins through chemical protein synthesis.Chem Sci,2017,8:1922-6
[28]Shchedrina VA,Zhang Y,Labunskyy VM,et al.Structurefunction relations,physiological roles,and evolution of mammalian ER-resident selenoproteins.Antioxid Redox Signal,2010,12:839-49
[29]Kim HY,Gladyshev VN.Methionine sulfoxide reductases:selenoprotein forms and roles in antioxidant protein repair in mammals.Biochem J,2007,407:321-9
[30]Addinsall AB,Wright CR,Andrikopoulos S,et al.Emerging roles of endoplasmic reticulum-resident selenoproteins in the regulation of cellular stress responses and the implications for metabolic disease.Biochem J,2018,475:1037-57
[31]Huang Z,Rose AH,Hoffmann PR.The role of selenium in inflammation and immunity:from molecular mechanisms to therapeutic opportunities.Antioxid Redox Signal,2012,16:705-43
[32]Yarilina A,Glimcher LH.TNF activates calcium-nuclear factor of activated T cells(NFAT)c1 signaling pathways in human macrophages.Proc Natl Acad Sci USA,2011,108:1573-8
[33]Zhang Y,Zhou Y,Schweizer U,et al.Comparative analysis of selenocysteine machinery and selenoproteome gene expression in mouse brain identifies neurons as key functional sites of selenium in mammals.J Biol Chem,2008,283:2427-38
[34]侯勤堂,刘琼.藻类硒富集与硒蛋白研究进展.微量元素与健康研究,2010,27:61-6
[35]Burk RF,Hill KE,Motley AK,et al.Deletion of selenoprotein pupregulates urinary selenium excretion and depresses whole-body selenium content.Biochim Biophys Acta,2006,1760:1789-93
[36]Nakayama A,Hill KE,Austin LM,et al.All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium.J Nutr,2007,137:690-3
[37]Mu?oz SS,Garner B,Ooi L.Understanding the role of ApoE fragments in Alzheimer's disease.Neurochem Res,2019,44:1297-305
[38]Schweizer U,Streckfuss F,Pelt P,et al.Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply.Biochem J,2005,386:221-6
[39]Burk RF,Hill KE,Motley AK,et al.Selenoprotein P and apolipoprotein E receptor-2 interact at the blood-brain barrier and also within the brain to maintain an essential selenium pool that protects against neurodegeneration.FASEB J,2014,28:3579-88
[40]Schweizer U,Brauer AU,Kohrle J,et al.Selenium and brain function:a poorly recognized liaison.Brain Res Rev,45:164-78
[41]Du X,Qiu S,Wang Z,et al.Direct interaction between selenoprotein P and tubulin.Int J Mol Sci,2014,15:10199-214
[42]Myhre O,Utkilen H,Duale N,et al.Metal dyshomeostasis and inflammation in Alzheimer’s and Parkinson’s diseases:possible impact of environmental exposures.Oxid Med Cell Longev,2013,2013:726954
[43]Chang LC,Shim MS,Chung J,et al.G-rich,a Drosophila selenoprotein,is a Golgi-resident type Ⅲ membrane protein.Biochem Biophys Res Commun,2006,348:1296-301
[44]Ben SB,Wang QY,Xia L,et al.Selenoprotein dSelK in Drosophila elevates release of Ca2+from endoplasmic reticulum by upregulating expression of inositol 1,4,5-trisphosphate receptor.Biochemistry(Mosc),2011,76:1030-6
[45]Ben SB,Peng B,Wang GC,et al.Overexpression of selenoprotein SelK in BGC-823 cells inhibits cell adhesion and migration.Biochemistry(Mosc),2015,80:1344-53
[46]Lescure A,Gautheret D,Carbon P,et al.Novel selenoproteins identified in silico and in vivo by using a conserved RNA structural motif.J Biol Chem,1999,274:38147-54
[47]Weissbach H,Resnick L,Brot N.Methionine sulfoxide reductases:history and cellular role in protecting against oxidative damage.Biochim Biophys Acta,2005,1703:203-12
[48]Oien DB,Moskovitz J.Selenium and the methionine sulfoxide reductase system.Molecules,2009,14:2337-44
[49]Jia Y,Zhou J,Liu H,et al.Effect of methionine sulfoxide reductase B1(Sel R)gene silencing on peroxynitrite-induced F-actin disruption in human lens epithelial cells.Biochem Biophys Res Commun,2014,443:876-81
[50]Chen P,Wang C,Ma XJ,et al.Direct interaction of selenoprotein R with clusterin and its possible role in Alzheimer's disease.PLoS One,2013,8:1-12
[51]Dumoulin M,Dobson CM.Probing the origins diagnosis and treatment of amyloid diseases using antibodies.Biochimie,2004,86:589-600
[52]韩莉欣,熊咏民.硒蛋白W生物学功能及其与疾病关系的研究进展.国外医学医学地理分册,2015,3:182-5
[53]Wang XL,Yang CP,Xu K,et al.Selenoprotein Wdepletion in vitro might indicate that its main function is not as an antioxidative enzyme.Biochemistry(Mosc),2010,75:201-7
[54]Raman AV,Pitts MW,Seyedali A,et al.Selenoprotein Wexpression and regulation in mouse brain and neurons.Brain Behav,2014,3:562-74
[55]Jeon YH,Yong HP,Kwon JH,et al.Inhibition of 14-3-3binding to Rictor of mTORC2 for Akt phosphorylation at Ser473 is regulated by selenoprotein W.BBA-Mol Cell Res,2013,1833:2135-42
[56]Jung CH,Jun CB,Ro SH,et al.ULK-Atg13-FIP200complexes mediate mTOR signaling to the autophagy machinery.Mol Biol Cell,2009,20:1992-2003
[57]Sarkar S,Ravikumar B,Floto RA,et al.Rapamycin and mTOR-independent autophagy inducers ameliorate toxicity of polyglutamine-expanded huntingtin and related proteinopathies.Cell Death Differ,2009,16:46-56
[58]Hatfield DL,Gladyshev VN.How selenium has altered our understanding of the genetic code.Mol Cell Biol,2002,22:3565-76
[59]Gao Y,Feng HC,Walder K,et al.Regulation of the selenoprotein SelS by glucose deprivation and endoplasmic reticulum stress-SelS is a novel glucose-regulated protein.FEBS Lett,2004,563:185-90
[60]Du JL,An LJ,Sun CK,et al.Overexpressing SelS may protect human umbilical vein endothelial cells from injuring by H2O2.Prog Biochem Biophys,2007,34:425-30
[61]Curran JE,Jowett JB,Elliott KS,et al.Genetic variation in selenoprotein S influences inflammatory response.Nat Genet,2005,37:1234-41
[62]Gao Y,Hannan NR,Wanyonyi S,et al.Activation of the selenoprotein SEPS1 gene expression by pro-inflammatory cytokines in HepG2 cells.Cytokine,2006,33:246-51
[63]Liu LX,Zhou XY,Li CS,et al.Selenoprotein S expression in the rat brain following focal cerebral ischemia.J Neurol Sci,2013,34:1671-8
[64]Jang JK,Park KJ,Lee JH,et al.Selenoprotein S is required for clearance of C99 through endoplasmic reticulum-associated degradation.Biochem Biophys Res Commun,2017,486:444-50
[65]Rueli RH,Torres DJ,Dewing AS,et al.Selenoprotein Sreduces endoplasmic reticulum stress-induced phosphorylation of Tau:potential role in selenate mitigation of Tau pathology.J Alzheimers Dis,2017,55:749-62
[66]Novoselov SV,Kryukov GV,Xu XM,et al.Selenoprotein H is a nucleolar thioredoxin-like protein with a unique expression pattern.J Biol Chem,2007,282:11960-8
[67]Mendelev N,Mehta SL,Witherspoon S,et al.Upregulation of human selenoprotein H in murine hippocampal neuronal cells promotes mitochondrial biogenesis and functional performance.Mitochondrion,2011,11:76-82
[68]Mehta SL,Mendelev N,Kumari S,et al.Overexpression of human selenoprotein H in neuronal cells enhances mitochondrial biogenesis and function through activation of protein kinase A,protein kinase B,and cyclic adenosine monophosphate response element-binding protein pathway.Int J Biochem Cell Biol,2013,45:604-11
[69]Wu RT,Cao L,Chen BP,et al.Selenoprotein H suppresses cellular senescence through genome maintenance and redox regulation.J Biol Chem,2014,289:34378-88
[70]Korotkov KV,Novoselov SV,Hatfield DL,et al.Mammalian selenoprotein in which selenocysteine(Sec)incorporation is supported by a new form of Sec insertion sequence element.Mol Cell Biol,2002,22:1402-11
[71]Battin EE,Brumaghim JL.Antioxidant activity of sulfur and selenium:a review of reactive oxygen species scavenging,glutathione peroxidase,and metal-binding antioxidant mechanisms.Cell Biochem Biophys,2009,55:1-23
[72]Mattson MP.Cellular actions ofβ-amyloid precursor protein and its soluble and fibrillogenic derivatives.Physiol Rev,1997,77:1081-132
[73]Reeves MA,Bellinger FP,Berry MJ.The neuroprotective functions of selenoprotein M and its role in cytosolic calcium regulation.Antioxid Redox Sign,2010,12:809-18
[74]Laferla FM.Calcium dyshomeostasis and intracellular signalling in Alzheimer's disease.Nat Rev Neurosci,2002,3:862-72
[75]Yim SY,Chae KR,Shim SB,et al.ERK activation induced by selenium treatment significantly downregulatesβ/γ-secretase activity and Tau phosphorylation in the transgenic rat overexpressing human selenoprotein M.Int J Mol Med,2009,24:91-6
[76]Pillai R,Uyehara-Lock JH,Bellinger FP.Selenium and selenoprotein function in brain disorders.IUBMB Life,2014,66:229-39
[77]Seiler A,Schneider M,F?rster H,et al.Glutathione peroxidase 4 senses and translates oxidative stress into12/15-lipoxygenase dependent-and AIF-mediated cell death.Cell Metab,2008,8:237-48
[78]Chen L,Na R,Gu M,et al.Lipid peroxidation upregulates BACE1 expression in vivo:a possible early event of amyloidogenesis in Alzheimer's disease.JNeurochem,2010,107:197-207
[79]Crack PJ,Cimdins K,Ali U,et al.Lack of glutathione peroxidase-1 exacerbates Aβ-mediated neurotoxicity in cortical neurons.J Neural Transm,2006,113:645-57
[80]Silvaadaya D,Gonsebatt ME,Guevara J.Thioredoxin system regulation in the central nervous system:experimental models and clinical evidence.Oxid Med Cell Longev,2014,2014:590808
[81]Kudin AP,Augustynek B,Lehmann AK,et al.The contribution of thioredoxin-2 reductase and glutathione peroxidase to H2O2 detoxification of rat brain mitochondria.Biochim Biophys Acta,2012,1817:1901-6
[82]郭咏梅,张博綦,闫素梅.硒对脂多糖诱导的奶牛乳腺上皮细胞氧化损伤的保护作用.动物营养学报,2017,29:3375-84
[2]赵娟.BACE基因在阿尔兹海默症中作用机制的研究[D].北京:北京理工大学,2008
[3]Hort J,O'Brien JT,Gainotti G,et al.EFNS guidelines for the diagnosis and management of Alzheimer's disease.Eur J Neurol,2010,17:1236-48
[4]赵丽波,付宏娟,张健莉.阿尔茨海默病发生机制的研究进展.中国老年学,2011,31:4997-8
[5]马云峰,王湘庆,郎森阳.微管相关蛋白Tau蛋白及Tau病的研究进展.解放军医学院学报,2015,36:621-4
[6]王玲,朱鸣峰.阿尔茨海默病发病机制的研究进展.吉林医学,2013,34:531-2
[7]Sakono M,Zako T.Amyloid oligomers:formation and toxicity of Aβoligomers.FEBS J,2010,277:1348-58
[8]Cardoso BR,Roberts BR,Bush AI,et al.Selenium,selenoproteins and neurodegenerative diseases.Metallomics,2015,7:1213-28
[9]Cheignon C,Tomas M,Bonnefont-Rousselot D,et al.Oxidative stress and the amyloidβpeptide in Alzheimer's disease.Redox Biol,2018,14:450-64
[10]Nesi G,Sestito S,Digiacomo M,et al.Oxidative stress,mitochondrial abnormalities and proteins deposition:multitarget approaches in Alzheimer's disease.Curr Top Med Chem,2017,17:3062-79
[11]刘晓杰,杨威,祁金顺.氧化应激与阿尔茨海默病.生理学报,2012,64:87-95
[12]Steffen J,Krohn M,Schwitlick C,et al.Expression of endogenous mouse APP modulatesβ-amyloid deposition in hAPP-transgenic mice.Acta Neuropathol Commun,2017,5:49
[13]Sastre M,Walter J,Gentleman SM.Interactions between APP secretases and inflammatory mediators.J Neuroinflamm,2008,5:1-11
[14]Marco LY,Venneri A,Farkas E,et al.Vascular dysfunction in the pathogenesis of Alzheimer's disease-A review of endothelium-mediated mechanisms and ensuing vicious circles.Neurobiol Dis,2015,82:593-606
[15]Mcinerney MP,Short JL,Nicolazzo JA.Neurovascular alterations in Alzheimer’s disease:transporter expression profiles and CNS drug access.AAPS J,2017,19:940-56
[16]Kivipelto M,Nqandu T,Fratiqlioni L,et al.Obesity and vascular risk factors at midlife and the risk of dementia and Alzheimer disease.Arch Neurol,2005,62:1556-60
[17]Hokama M,Oka S,Leon J,et al.Altered expression of diabetes-related genes in Alzheimer’s disease brains:the Hisayama study.Cereb Cortex,2014,24:2476-88
[18]Li J,Liu D,Sun L,et al.Advanced glycation end products and neurodegenerative diseases:mechanisms and perspective.J Neurol Sci,2012,317:1-5
[19]陈长兰,郇丰宁,孟雪莲.硒对人体的作用机理及科学补硒方法.辽宁大学学报(自然科学版),2016,43:155-68
[20]Dominiak A,Wilkaniec A,J??ko H,et al.Selol,an organic selenium donor,prevents lipopolysaccharide-induced oxidative stress and inflammatory reaction in the rat brain.Neurochem Int,2017,108:66-77
[21]Aaseth J,Alexander J,Bj?rklund G,et al.Treatment strategies in Alzheimer's disease:a review with focus on selenium supplementation.Biometals,2016,29:827-39
[22]Nakayama A,Hill KE,Austin LM,et al.All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium.Eur J Nutr,2007,137:690-3
[23]Schweizer U,Streckfuss F,Pelt P,et al.Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply.Biochem J,2005,386:221-6
[24]Rita CB,Silva BV,Jacob FW,et al.Selenium status in elderly:relation to cognitive decline.J Trace Elem Med Biol,2014,28:422-6
[25]Olde Rikkert MG,Verhey FR,Sijben JW,et al.Differences in nutritional status between very mild Alzheimer's disease patients and healthy controls.J Alzheimers Dis,2014,41:261-71
[26]Kryukov GV,Castellano S,Novoselov SV,et al.Characterization of mammalian selenoproteomes.Science,2003,300:1439-43
[27]Dery L,Reddy PS,Dery S,et al.Accessing human selenoproteins through chemical protein synthesis.Chem Sci,2017,8:1922-6
[28]Shchedrina VA,Zhang Y,Labunskyy VM,et al.Structurefunction relations,physiological roles,and evolution of mammalian ER-resident selenoproteins.Antioxid Redox Signal,2010,12:839-49
[29]Kim HY,Gladyshev VN.Methionine sulfoxide reductases:selenoprotein forms and roles in antioxidant protein repair in mammals.Biochem J,2007,407:321-9
[30]Addinsall AB,Wright CR,Andrikopoulos S,et al.Emerging roles of endoplasmic reticulum-resident selenoproteins in the regulation of cellular stress responses and the implications for metabolic disease.Biochem J,2018,475:1037-57
[31]Huang Z,Rose AH,Hoffmann PR.The role of selenium in inflammation and immunity:from molecular mechanisms to therapeutic opportunities.Antioxid Redox Signal,2012,16:705-43
[32]Yarilina A,Glimcher LH.TNF activates calcium-nuclear factor of activated T cells(NFAT)c1 signaling pathways in human macrophages.Proc Natl Acad Sci USA,2011,108:1573-8
[33]Zhang Y,Zhou Y,Schweizer U,et al.Comparative analysis of selenocysteine machinery and selenoproteome gene expression in mouse brain identifies neurons as key functional sites of selenium in mammals.J Biol Chem,2008,283:2427-38
[34]侯勤堂,刘琼.藻类硒富集与硒蛋白研究进展.微量元素与健康研究,2010,27:61-6
[35]Burk RF,Hill KE,Motley AK,et al.Deletion of selenoprotein pupregulates urinary selenium excretion and depresses whole-body selenium content.Biochim Biophys Acta,2006,1760:1789-93
[36]Nakayama A,Hill KE,Austin LM,et al.All regions of mouse brain are dependent on selenoprotein P for maintenance of selenium.J Nutr,2007,137:690-3
[37]Mu?oz SS,Garner B,Ooi L.Understanding the role of ApoE fragments in Alzheimer's disease.Neurochem Res,2019,44:1297-305
[38]Schweizer U,Streckfuss F,Pelt P,et al.Hepatically derived selenoprotein P is a key factor for kidney but not for brain selenium supply.Biochem J,2005,386:221-6
[39]Burk RF,Hill KE,Motley AK,et al.Selenoprotein P and apolipoprotein E receptor-2 interact at the blood-brain barrier and also within the brain to maintain an essential selenium pool that protects against neurodegeneration.FASEB J,2014,28:3579-88
[40]Schweizer U,Brauer AU,Kohrle J,et al.Selenium and brain function:a poorly recognized liaison.Brain Res Rev,45:164-78
[41]Du X,Qiu S,Wang Z,et al.Direct interaction between selenoprotein P and tubulin.Int J Mol Sci,2014,15:10199-214
[42]Myhre O,Utkilen H,Duale N,et al.Metal dyshomeostasis and inflammation in Alzheimer’s and Parkinson’s diseases:possible impact of environmental exposures.Oxid Med Cell Longev,2013,2013:726954
[43]Chang LC,Shim MS,Chung J,et al.G-rich,a Drosophila selenoprotein,is a Golgi-resident type Ⅲ membrane protein.Biochem Biophys Res Commun,2006,348:1296-301
[44]Ben SB,Wang QY,Xia L,et al.Selenoprotein dSelK in Drosophila elevates release of Ca2+from endoplasmic reticulum by upregulating expression of inositol 1,4,5-trisphosphate receptor.Biochemistry(Mosc),2011,76:1030-6
[45]Ben SB,Peng B,Wang GC,et al.Overexpression of selenoprotein SelK in BGC-823 cells inhibits cell adhesion and migration.Biochemistry(Mosc),2015,80:1344-53
[46]Lescure A,Gautheret D,Carbon P,et al.Novel selenoproteins identified in silico and in vivo by using a conserved RNA structural motif.J Biol Chem,1999,274:38147-54
[47]Weissbach H,Resnick L,Brot N.Methionine sulfoxide reductases:history and cellular role in protecting against oxidative damage.Biochim Biophys Acta,2005,1703:203-12
[48]Oien DB,Moskovitz J.Selenium and the methionine sulfoxide reductase system.Molecules,2009,14:2337-44
[49]Jia Y,Zhou J,Liu H,et al.Effect of methionine sulfoxide reductase B1(Sel R)gene silencing on peroxynitrite-induced F-actin disruption in human lens epithelial cells.Biochem Biophys Res Commun,2014,443:876-81
[50]Chen P,Wang C,Ma XJ,et al.Direct interaction of selenoprotein R with clusterin and its possible role in Alzheimer's disease.PLoS One,2013,8:1-12
[51]Dumoulin M,Dobson CM.Probing the origins diagnosis and treatment of amyloid diseases using antibodies.Biochimie,2004,86:589-600
[52]韩莉欣,熊咏民.硒蛋白W生物学功能及其与疾病关系的研究进展.国外医学医学地理分册,2015,3:182-5
[53]Wang XL,Yang CP,Xu K,et al.Selenoprotein Wdepletion in vitro might indicate that its main function is not as an antioxidative enzyme.Biochemistry(Mosc),2010,75:201-7
[54]Raman AV,Pitts MW,Seyedali A,et al.Selenoprotein Wexpression and regulation in mouse brain and neurons.Brain Behav,2014,3:562-74
[55]Jeon YH,Yong HP,Kwon JH,et al.Inhibition of 14-3-3binding to Rictor of mTORC2 for Akt phosphorylation at Ser473 is regulated by selenoprotein W.BBA-Mol Cell Res,2013,1833:2135-42
[56]Jung CH,Jun CB,Ro SH,et al.ULK-Atg13-FIP200complexes mediate mTOR signaling to the autophagy machinery.Mol Biol Cell,2009,20:1992-2003
[57]Sarkar S,Ravikumar B,Floto RA,et al.Rapamycin and mTOR-independent autophagy inducers ameliorate toxicity of polyglutamine-expanded huntingtin and related proteinopathies.Cell Death Differ,2009,16:46-56
[58]Hatfield DL,Gladyshev VN.How selenium has altered our understanding of the genetic code.Mol Cell Biol,2002,22:3565-76
[59]Gao Y,Feng HC,Walder K,et al.Regulation of the selenoprotein SelS by glucose deprivation and endoplasmic reticulum stress-SelS is a novel glucose-regulated protein.FEBS Lett,2004,563:185-90
[60]Du JL,An LJ,Sun CK,et al.Overexpressing SelS may protect human umbilical vein endothelial cells from injuring by H2O2.Prog Biochem Biophys,2007,34:425-30
[61]Curran JE,Jowett JB,Elliott KS,et al.Genetic variation in selenoprotein S influences inflammatory response.Nat Genet,2005,37:1234-41
[62]Gao Y,Hannan NR,Wanyonyi S,et al.Activation of the selenoprotein SEPS1 gene expression by pro-inflammatory cytokines in HepG2 cells.Cytokine,2006,33:246-51
[63]Liu LX,Zhou XY,Li CS,et al.Selenoprotein S expression in the rat brain following focal cerebral ischemia.J Neurol Sci,2013,34:1671-8
[64]Jang JK,Park KJ,Lee JH,et al.Selenoprotein S is required for clearance of C99 through endoplasmic reticulum-associated degradation.Biochem Biophys Res Commun,2017,486:444-50
[65]Rueli RH,Torres DJ,Dewing AS,et al.Selenoprotein Sreduces endoplasmic reticulum stress-induced phosphorylation of Tau:potential role in selenate mitigation of Tau pathology.J Alzheimers Dis,2017,55:749-62
[66]Novoselov SV,Kryukov GV,Xu XM,et al.Selenoprotein H is a nucleolar thioredoxin-like protein with a unique expression pattern.J Biol Chem,2007,282:11960-8
[67]Mendelev N,Mehta SL,Witherspoon S,et al.Upregulation of human selenoprotein H in murine hippocampal neuronal cells promotes mitochondrial biogenesis and functional performance.Mitochondrion,2011,11:76-82
[68]Mehta SL,Mendelev N,Kumari S,et al.Overexpression of human selenoprotein H in neuronal cells enhances mitochondrial biogenesis and function through activation of protein kinase A,protein kinase B,and cyclic adenosine monophosphate response element-binding protein pathway.Int J Biochem Cell Biol,2013,45:604-11
[69]Wu RT,Cao L,Chen BP,et al.Selenoprotein H suppresses cellular senescence through genome maintenance and redox regulation.J Biol Chem,2014,289:34378-88
[70]Korotkov KV,Novoselov SV,Hatfield DL,et al.Mammalian selenoprotein in which selenocysteine(Sec)incorporation is supported by a new form of Sec insertion sequence element.Mol Cell Biol,2002,22:1402-11
[71]Battin EE,Brumaghim JL.Antioxidant activity of sulfur and selenium:a review of reactive oxygen species scavenging,glutathione peroxidase,and metal-binding antioxidant mechanisms.Cell Biochem Biophys,2009,55:1-23
[72]Mattson MP.Cellular actions ofβ-amyloid precursor protein and its soluble and fibrillogenic derivatives.Physiol Rev,1997,77:1081-132
[73]Reeves MA,Bellinger FP,Berry MJ.The neuroprotective functions of selenoprotein M and its role in cytosolic calcium regulation.Antioxid Redox Sign,2010,12:809-18
[74]Laferla FM.Calcium dyshomeostasis and intracellular signalling in Alzheimer's disease.Nat Rev Neurosci,2002,3:862-72
[75]Yim SY,Chae KR,Shim SB,et al.ERK activation induced by selenium treatment significantly downregulatesβ/γ-secretase activity and Tau phosphorylation in the transgenic rat overexpressing human selenoprotein M.Int J Mol Med,2009,24:91-6
[76]Pillai R,Uyehara-Lock JH,Bellinger FP.Selenium and selenoprotein function in brain disorders.IUBMB Life,2014,66:229-39
[77]Seiler A,Schneider M,F?rster H,et al.Glutathione peroxidase 4 senses and translates oxidative stress into12/15-lipoxygenase dependent-and AIF-mediated cell death.Cell Metab,2008,8:237-48
[78]Chen L,Na R,Gu M,et al.Lipid peroxidation upregulates BACE1 expression in vivo:a possible early event of amyloidogenesis in Alzheimer's disease.JNeurochem,2010,107:197-207
[79]Crack PJ,Cimdins K,Ali U,et al.Lack of glutathione peroxidase-1 exacerbates Aβ-mediated neurotoxicity in cortical neurons.J Neural Transm,2006,113:645-57
[80]Silvaadaya D,Gonsebatt ME,Guevara J.Thioredoxin system regulation in the central nervous system:experimental models and clinical evidence.Oxid Med Cell Longev,2014,2014:590808
[81]Kudin AP,Augustynek B,Lehmann AK,et al.The contribution of thioredoxin-2 reductase and glutathione peroxidase to H2O2 detoxification of rat brain mitochondria.Biochim Biophys Acta,2012,1817:1901-6
[82]郭咏梅,张博綦,闫素梅.硒对脂多糖诱导的奶牛乳腺上皮细胞氧化损伤的保护作用.动物营养学报,2017,29:3375-84