脊髓损伤后胶质瘢痕形成的研究进展

doi:10.3969/j.issn.1006-9771.2018.06.004

摘要/Abstract

摘要： 脊髓损伤后,胶质瘢痕的形成主要涉及星形胶质细胞肥大、增殖、迁移以及表达的胶质纤维酸性蛋白、波形蛋白和巢蛋白的增加等多个过程,并且影响神经元轴突的生长。

Abstract: After spinal cord injury, the formation of glial scar related to the hypertrophy, proliferation and migration of astrocytes, and the increased expression of glial fibers acidic protein, vimentin and nestin, etc., and it may also inhibit the growth of neuron axon.

Key words: spinal cord injury, glial scar, astrocytes, review

中图分类号:

R651.2

巩朝阳,刘开鑫,向高,张海鸿. 脊髓损伤后胶质瘢痕形成的研究进展[J]. 《中国康复理论与实践》, 2018, 24(6): 641-644.

GONG Chao-yang, LIU Kai-xin, XIANG Gao, ZHANG Hai-hong. Advance in Glial Scar Formation after Spinal Cord Injury (review)[J]. 《Chinese Journal of Rehabilitation Theory and Practice》, 2018, 24(6): 641-644.

参考文献

[1] Bradbury EJ, Moon LD, Popat RJ, et al.Chondroitinase ABC promotes functional recovery after spinal cord injury[J]. Nature, 2002, 416(6881): 636-640.
[2] Yuan YM, He C.The glial scar in spinal cord injury and repair[J]. Neurosci Bull, 2013, 29(4): 421-435.
[3] Karimi-Abdolrezaee S, Billakanti R.Reactive astrogliosis after spinal cord injury-beneficial and detrimental effects[J]. Mol Neurobiol, 2012, 46(2): 251-264.
[4] Sofroniew MV, Vinters HV.Astrocytes: biology and pathology[J]. Acta Neuropathol, 2010, 119(1): 7-35.
[5] Seifert G, Schilling K, Steinhäuser C.Astrocyte dysfunction in neurological disorders: a molecular perspective[J]. Nat Rev Neurosci, 2006, 7(3): 194-206.
[6] Sofroniew MV.Molecular dissection of reactive astrogliosis and glial scar formation[J]. Trends Neurosci, 2009, 32(12): 638-647.
[7] Anderson MA, Burda JE, Ren Y, et al.Astrocyte scar formation aids central nervous system axon regeneration[J]. Nature, 2016, 532(7598): 195-200.
[8] Zhao JW, Raha-Chowdhury R, Fawcett JW, et al.Astrocytes and oligodendrocytes can be generated from NG2<sup>+</sup> progenitors after acute brain injury: intracellular localization of oligodendrocyte transcription factor 2 is associated with their fate choice[J]. Eur J Neurosci, 2009, 29(9): 1853-1869.
[9] Renault-Mihara F, Okada S, Shibata S, et al.Spinal cord injury: emerging beneficial role of reactive astrocytes' migration[J]. Int J Biochem Cell Biol, 2008, 40(9): 1649-1653.
[10] Halassa MM, Fellin T, Haydon PG.The tripartite synapse: roles for gliotransmission in health and disease[J]. Trends Mol Med, 2007, 13(2): 54-63.
[11] Perea G, Navarrete M, Araque A.Tripartite synapses: astrocytes process and control synaptic information[J]. Trends Neurosci, 2009, 32(8): 421-431.
[12] Pellerin L, Bouzier-Sore AK, Aubert A, et al.Activity-dependent regulation of energy metabolism by astrocytes: an update[J]. Glia, 2007, 55(12): 1251-1262.
[13] Chung WS, Allen NJ, Eroglu C.Astrocytes control synapse formation, function, and elimination[J]. Cold Spring Harb Perspect Biol, 2015, 7(9): a020370.
[14] Pekny M, Pekna M.Astrocyte reactivity and reactive astrogliosis: costs and benefits[J]. Physiol Rev, 2014, 94(4): 1077-1098.
[15] Liddelow SA, Barres BA.Reactive astrocytes: production, function, and therapeutic potential[J]. Immunity, 2017, 46(6): 957-967.
[16] Pekny M, Pekna M.Astrocyte intermediate filaments in CNS pathologies and regeneration[J]. J Pathol, 2004, 204(4): 428-437.
[17] Calvo JL, Carbonell AL, Boya J.Co-expression of glial fibrillary acidic protein and vimentin in reactive astrocytes following brain injury in rats[J]. Brain Res, 1991, 566(1-2): 333-336.
[18] Fawcett JW.Astrocytic and neuronal factors affecting axon regeneration in the damaged central nervous system[J]. Cell Tissue Res, 1997, 290(2): 371-377.
[19] Pekny M, Levéen P, Pekna M, et al.Mice lacking glial fibrillary acidic protein display astrocytes devoid of intermediate filaments but develop and reproduce normally[J]. EMBO J, 1995, 14(8): 1590-1598.
[20] Herrmann JE, Imura T, Song B, et al.STAT3 is a critical regulator of astrogliosis and scar formation after spinal cord injury[J]. J Neurosci, 2008, 28(28): 7231-7243.
[21] Wanner IB, Anderson MA, Song B, et al.Glial scar borders are formed by newly proliferated, elongated astrocytes that interact to corral inflammatory and fibrotic cells via STAT3-dependent mechanisms after spinal cord injury[J]. J Neurosci, 2013, 33(31): 12870-12886.
[22] Hong P, Jiang M, Li H.Functional requirement of dicer1 and miR-17-5p in reactive astrocyte proliferation after spinal cord injury in the mouse[J]. Glia, 2014, 62(12): 2044-2060.
[23] Chen J, Cui Z, Yang S, et al.The upregulation of annexin A2 after spinal cord injury in rats may have implication for astrocyte proliferation[J]. Neuropeptides, 2017, 61: 67-76.
[24] Wang HH, Hsieh HL, Wu CY, et al.Endothelin-1 enhances cell migration via matrix metalloproteinase-9 up-regulation in brain astrocytes[J]. J Neurochem, 2010, 113(5): 1133-1149.
[25] Koyama Y, Takemura M, Fujiki K, et al.BQ788, an endothelin ET(B) receptor antagonist, attenuates stab wound injury-induced reactive astrocytes in rat brain[J]. Glia, 1999, 26(3): 268-271.
[26] Wang SM, Hsu JC, Ko CY, et al.Astrocytic CCAAT/enhancer-binding protein delta contributes to glial scar formation and impairs functional recovery after spinal cord injury[J]. Mol Neurobiol, 2016, 53(9): 5912-5927.
[27] Zhou K, Nan W, Feng D, et al.Spatiotemporal expression of Ski after rat spinal cord injury[J]. Neuroreport, 2017, 28(3): 149-157.
[28] Zhao X, Wang XW, Zhou KS, et al.Expression of Ski and its role in astrocyte proliferation and migration[J]. Neuroscience, 2017, 362: 1-12.
[29] Zhao X, Zhou KS, Li ZH, et al.Knockdown of Ski decreased the reactive astrocytes proliferation in vitro induced by oxygen-glucose deprivation/reoxygenation[J]. J Cell Biochem, 2018, 119(6): 4548-4558.
[30] Coulson-Thomas VJ, Lauer ME, Soleman S, et al.Tumor necrosis factor-stimulated gene-6 (TSG-6) is constitutively expressed in adult central nervous system (CNS) and associated with astrocyte-mediated glial scar formation following spinal cord injury[J]. J Biol Chem, 2016, 291(38): 19939-19952.
[31] Chen X, Chen C, Hao J, et al.Effect of CLIP3 upregulation on astrocyte proliferation and subsequent glial scar formation in the rat spinal cord via stat3 pathway after injury[J]. J Mol Neurosci, 2018, 64(1): 117-128.
[32] Lang BT, Cregg JM, DePaul MA, et al. Modulation of the proteoglycan receptor PTPσ promotes recovery after spinal cord injury[J]. Nature, 2015, 518(7539): 404-408.
[33] Vadivelu S, Stewart TJ, Qu Y, et al.NG2<sup>+</sup> progenitors derived from embryonic stem cells penetrate glial scar and promote axonal outgrowth into white matter after spinal cord injury[J]. Stem Cells Transl Med, 2015, 4(4): 401-411.
[34] Lee JK, Chow R, Xie F, et al.Combined genetic attenuation of myelin and semaphorin-mediated growth inhibition is insufficient to promote serotonergic axon regeneration[J]. J Neurosci, 2010, 30(32): 10899-10904.
[35] Sun F, Park KK, Belin S, et al.Sustained axon regeneration induced by co-deletion of PTEN and SOCS3[J]. Nature, 2011, 480(7377): 372-375.
[36] Zukor K, Belin S, Wang C, et al.Short hairpin RNA against PTEN enhances regenerative growth of corticospinal tract axons after spinal cord injury[J]. J Neurosci, 2013, 33(39): 15350-15361.
[37] Pekny M, Wilhelmsson U, Pekna M.The dual role of astrocyte activation and reactive gliosis[J]. Neurosci Lett, 2014, 565: 30-38.
[38] Zou Y, Stagi M, Wang X, et al.Gene-silencing screen for mammalian axon regeneration identifies Inpp5f (Sac2) as an endogenous suppressor of repair after spinal cord injury[J]. J Neurosci, 2015, 35(29): 10429-10439.
[39] Hu J, Zhang G, Rodemer W, et al.The role of RhoA in retrograde neuronal death and axon regeneration after spinal cord injury[J]. Neurobiol Dis, 2017, 98: 25-35.