少突胶质细胞在神经退行性疾病中的研究进展
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摘要
少突胶质细胞是中枢神经系统中一群高度特化的神经胶质细胞,由少突胶质前体细胞分化形成,其主要功能是提供髓鞘,维持轴突的完整性.早期对少突胶质细胞的研究主要集中在少突胶质前体细胞的形成机制及其分化为少突胶质细胞的过程;最近的研究侧重于对少突胶质前体细胞/少突胶质细胞参与神经退行性疾病的发病过程以及神经系统损伤修复过程.文章综述了少突胶质细胞的功能和分化发育,及其在肌萎缩侧索硬化、阿尔茨海默病、亨廷顿舞蹈病和多发性硬化中的作用.
Oligodendrocytes are a group of highly specialized glial cells in the central nervous system. They are differentiated from oligodendrocyte precursor cells. Their main functions are to provide myelin and maintain the integrity of the axons. Early studies of oligodendrocyte cells mainly focused on the origin of oligodendrocyte precursor cells and the mechanism of their differentiation into oligodendrocyte. Currently, more attention about the oligodendrocyte cells are paid on the roles of oligodendrocyte precursor cells/oligodendrocyte in the pathogenesis of neurodegenerative diseases and the repair of neurological damage. This article discussed the function and differentiation of oligodendrocytes, as well as their role in amyotrophic lateral sclerosis, Alzheimer's disease,Huntington's disease and multiple sclerosis.
Oligodendrocytes are a group of highly specialized glial cells in the central nervous system. They are differentiated from oligodendrocyte precursor cells. Their main functions are to provide myelin and maintain the integrity of the axons. Early studies of oligodendrocyte cells mainly focused on the origin of oligodendrocyte precursor cells and the mechanism of their differentiation into oligodendrocyte. Currently, more attention about the oligodendrocyte cells are paid on the roles of oligodendrocyte precursor cells/oligodendrocyte in the pathogenesis of neurodegenerative diseases and the repair of neurological damage. This article discussed the function and differentiation of oligodendrocytes, as well as their role in amyotrophic lateral sclerosis, Alzheimer's disease,Huntington's disease and multiple sclerosis.
引文
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[2]Liang H,Wu C,Deng Y,et al.Aldehyde dehydrogenases 1A2 expression and distributionare potentially associated with neuron death in spinal cord of Tg(SOD1*G93A)1Gur mice[J].International Journal of Biological Sciences,2017,13(5):574-587.DOI:10.7150/ijbs.19150.
[3]Kang S H,Li Y,Fukaya M,et al.Degeneration and impaired regeneration of gray matter oligodendrocytes in amyotrophic lateral sclerosis[J].Nature Neuroscience,2013,16(5):571-579.DOI:10.1038/nn.3357.
[4]Jeffries M A,Urbanek K,Torres L,et al.ERK1/2 Activation in preexisting oligodendrocytes of adult mice drives new myelin synthesis and enhanced CNS function[J].Journal of Neuroscience the Official Journal of the Society for Neuroscience,2016,36(35):9 186-9 200.DOI:10.1523/JNEUROSCI.1444-16.2016.
[5]Sampaio-Baptista C,Johansen-Berg H.White matter plasticity in the adult brain[J].Neuron,2017,96(6):1 239-1 251.DOI:10.1016/j.neuron.2017.11.026.
[6]Mckenzie I A,Ohayon D,Li H,et al.Motor skill learning requires active central myelination[J].Science,2014,346(6207):318-322.DOI:10.1126/science.1254960.
[7]Keiner S,Niv F,Neumann S,et al.Effect of skilled reaching training and enriched environment on generation of oligodendrocytes in the adult sensorimotor cortex and corpus callosum[J].BMC Neuroscience,2017,18 (1):31.DOI:10.1186/s12868-017-0347-2.
[8]Lin X,Ohayon D,Mckenzie I A,et al.Rapid production of new oligodendrocytes is required in the earliest stages of motor-skill learning[J].Nature Neuroscience,2016,19(9):1 210-1 217.DOI:10.1038/nn.4351.
[9]Nave K A,Werner H B.Myelination of the nervous system:mechanisms and functions[J].Annu Rev Cell DevBiol,2014,30(1):503-533.DOI:10.1146/annurevcellbio-100913-013101.
[10]Chamberlain K A,Nanescu S E,Psachoulia K,et al.Oligodendrocyte regeneration:its significance in myelin replacement and neuroprotection in multiple sclerosis[J].Neuropharmacology,2016,110:633-643.DOI:10.1016/j.neuropharm.2015.10.010.
[11]Barateiro A,Fernandes A.Temporal oligodendrocyte lineage progression:in vitro models of proliferation,differentiation and myelination[J].Biochim Biophys Acta,2014,1843(9):1 917-1 929.
[12]Trias E,Ibarburu S,BarretoNú?ez R,et al.Significance of aberrant glial cell phenotypes in pathophysiology of amyotrophic lateral sclerosis[J].Neuroscience Letters,2016,636:27-31.
[13]Simons M,Lyons D A.Axonal selection and myelin sheath generation in the central nervous system[J].Current Opinion in Cell Biology,2013,25(4):512-519.DOI:10.1016/j.ceb.2013.04.007.
[14]Di P M,Phillpsh O R,Sanchez-Anchez-Castaneda C,et al.MRI measures of corpus callosum iron and myelin in early Huntington's disease[J].Human Brain Mapping,2014,35(7):3 143-3 151.DOI:10.1002/hbm.22391.
[15]Mctigue D M,Tripathi R B.The life,death,and replacement of oligodendrocytes in the adult CNS[J].Journal of Neurochemistry,2008,107(1):1-19.DOI:10.1111/jnc.2008.107.issue-1.
[16]Franklin R J M,Gallo V.The translational biology of remyelination:Past,present,and future[J].Glia,2014,62(11):1 905-1 915.DOI:10.1002/glia.22622.
[17]Hynd M R,Scott H L,Dodd P R.Glutamate-mediated excitotoxicity and neurodegenerationin Alzheimer's disease[J].Neurochemistry International,2004,45(5):583-595.DOI:10.1016/j.neuint.2004.03.007.
[18]Dan E,Wang L P,Klempin F,et al.Enriched environment and physical activity reduce microglia and influence the fate of NG2 cells in the amygdala of adult mice[J].Cell&Tissue Research,2011,345(1):69-86.
[19]Wang S,Young K M.White matter plasticity in adulthood[J].Neuroscience,2014,276(6):148-160.
[20]Aguirre A A,Chittajallu R,Belachew S,et al.NG2-expressing cells in the subventricular zone are type C-Like cells and contribute to interneuron generation in the postnatal hippocampus[J].Journal of Cell Biology,2004,165(4):575-589.DOI:10.1083/jcb.200311141.
[21]Tobim W O,Popescu B,Lowe V J,et al.Multiple sclerosis masquerading as alzheimer's type dementia:clinical,radiological,and pathological findings[J].MultScler,2016,10(4):698-704.
[22]Tes K H,Herrup K.Re-imagining Alzheimer's diseasethe diminishing importance of amyloid and a glimpse of what lies ahead[J].Journal of Neurochemistry,2017,143(4):432-444.DOI:10.1111/jnc.2017.143.issue-4.
[23]Huang B,Wei W,Wang G,et al.Mutant Huntingtindownregulates myelin regulatory factor-mediated myelin gene expression and affects mature oligodendrocytes[J].Neuron,2015,85(6):1 212-1 226.DOI:10.1016/j.neuron.2015.02.026.
[24]Boulanger J J,Messier C.From precursors to myelinatingoligodendrocytes:contribution of intrinsic and extrinsic factors to white matter plasticity in the adult brain[J].Neuroscience,2014,269(1):343-366.
[25]Rowland L P,Shneider N A.Amyotrophic lateral sclerosis[J].Current Opinion in Neurology,1994,7(4):310-315.DOI:10.1097/00019052-199408000-00006.
[26]Philips T,Bentoabreu A,Nonneman A,et al.Oligodendrocyte dysfunction in the pathogenesis of amyotrophic lateral sclerosis[J].Brain,2013,136(2):471-482.DOI:10.1093/brain/aws339.
[27]Lee Y,Brett M M,Li Y,et al.Oligodendroglia metabolically support axons and contribute to neurodegeneration[J].Nature,2012,487(7408):443-448.DOI:10.1038/nature11314.
[28]Morrison B M,Lee Y,Rothstein J D.Oligodendroglia:metabolic supporters of axons[J].Trends Cell,2013,23(12):644-651.DOI:10.1016/j.tcb.2013.07.007.
[29]Lu Y,Tang C,Zhu L,et al.The overexpression of TDP-43 protein in the neuron and oligodendrocyte cells causes the progressive motor neuron degeneration in the SOD1 G93A transgenic mouse model of amyotrophic lateral sclerosis[J].International Journal of Biological Sciences,2016,12(9):1 140-1 149.DOI:10.7150/ijbs.15938.
[30]Uchida T,Tamaki Y,Ayaki T,et al.CUL2-mediated clearance of misfolded TDP-43 is paradoxically affected by VHL in oligodendrocytes in ALS[J].Scientific Reports,2016,6:19 118.DOI:10.1038/srep19118.
[31]Cai Z,Xiao M.Oligodendrocytes and Alzheimer's disease[J].International Journal of Neuroscience,2016,126 (2):97-104.DOI:10.3109/00207454.2015.1025778.
[32]Horiuchi M,Maezawa I,Itoh A,et al.Amyloidβ1-42oligomer inhibits myelin sheet formation in vitro[J].Neurobiology of Aging,2012,33(3):499-509.DOI:10.1016/j.neurobiolaging.2010.05.007.
[33]Kavroulakis E,Simos P G,Kalaitzakis G,et al.Myelin content changes in probable Alzheimer's disease and mild cognitive impairment:Associations with age and severity of neuropsychiatric impairment[J].Journal of Magnetic Resonance Imaging Jmri,2018,47(5):1 359-1 372.DOI:10.1002/jmri.v47.5.
[34]Madabhushi R,Pan L,Tsai L H.DNA damage and its links toneurodegeneration[J].Neuron,2014,83(2):266-282.DOI:10.1016/j.neuron.2014.06.034.
[35]Wu Y,Ma Y,Liu Z,et al.Alterations of myelin morphology and oligodendrocyte development in early stage of Alzheimer’s disease mouse model[J].Neuroscience Letters,2017,642:102-106.DOI:10.1016/j.neulet.2017.02.007.
[36]Wu D,Tang X,Gu L H,et al.LINGO-1 antibody ameliorates myelin impairment and spatial memory deficits in the early stage of 5XFAD mice[J].Cns Neuroscience&Therapeutics,2018,24(5):381-393.
[37]Zhang L,Chao F L,Luo Y M,et al.Exercise prevents cognitive function decline and demyelination in the white matter of APP/PS1 transgenic AD mice[J].Current Alzheimer Research,2016,14(6):645-655.
[38]Phillips O,Squitieri F,Sanchezcastaneda C,et al.Deep white matter in Huntington's disease[J].Plos One,2014,9(10):e109676.DOI:10.1371/journal.pone.0109676.
[39]Peyron F,Timsit S,Thomas J L,et al.In situ expression of PLP/DM-20,MBP,and CNP during embryonic and postnatal development of the jimpy mutant and of transgenic mice overexpressing PLP[J].Journal of Neuroscience Research,2015,50(2):190-201.
[40]Xiang Z,Krainc D.Pharmacological upregulation of PGC1αin oligodendrocytes:implications for Huntington's disease[J].Journal of Huntingtons Disease,2013,2(1):101-105.
[41]Xiang Z,Valenza M,Cui L,et al.PGC1αcontributes to dysmyelination in experimental models of Huntington's disease[J].Journal of Neuroscience the Official Journal of the Society for Neuroscience,2011,31(26):9 544-9 553.DOI:10.1523/JNEUROSCI.1291-11.2011.
[42]Bartzokis G,Lu P H,Tishler T A,et al.Myelin breakdown and iron changes in Huntington's disease:Pathogenesis and treatment implications[J].Neurochemical Research,2007,32(10):1 655-1 664.DOI:10.1007/s11064-007-9352-7.
[43]Southwell A L,Franciosi S,Villanueva E B,et al.Antisemaphorin 4D immunotherapy ameliorates neuropathology and some cognitive impairment in the YAC128mouse model of Huntington disease[J].Neurobiology of Disease,2015,76:46-56.DOI:10.1016/j.nbd.2015.01.002.
[44]Lan M,Tang X,Zhang J,et al.Insights in pathogenesis of multiple sclerosis:nitric oxide may induce mitochondrial dysfunction of oligodendrocytes[J].Reviews in the Neurosciences,2018,29(1):39-53.
[45]Sun J J,Ren Q G,Xu L,et al.LINGO-1 antibody ameliorates myelin impairment and spatial memory deficits in experimental autoimmune encephalomyelitis mice[J].Sci Rep,2015,5:14 235.DOI:10.1038/srep14235.
[46]Ramanathan S,Dale R C,Brilot F.Anti-MOG antibody:The history,clinical phenotype,and pathogenicity of a serum biomarker for demyelination[J].Autoimmunity Reviews,2016,15(4):307-324.DOI:10.1016/j.autrev.2015.12.004.
[47]Pittock S J,Lucchinetti C F.The pathology of MS:new insights and potential clinical applications[J].Neurologist,2007,13(2):45-56.DOI:10.1097/01.nrl.0000253065.31662.37.
[48]Hecker M,Fitzner B,Wendt M,et al.High-density peptide microarray analysis of igg autoantibody reactivities in serum and cerebrospinal fluid of Multiple Sclerosis patients[J].Molecular&Cellular Proteomics Mcp,2016,15(4):1 360.
[49]O’Connor K C,Appel H,Bregoli L,et al.Antibodies from inflamed central nervous system tissue recognize myelin oligodendrocyte glycoprotein[J].Journal of Immunology,2005,175(3):1 974-1 982.DOI:10.4049/jimmunol.175.3.1974.
[50]Niehaus A,Shi J,Grzenkowski M,et al.Patients with active relapsing-remitting multiple sclerosis synthesize antibodies recognizing oligodendrocyte progenitor cell surface protein:Implications for remyelination[J].Annals of Neurology,2010,48(3):362-371.
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