《Chinese Journal of Rehabilitation Theory and Practice》 ›› 2018, Vol. 24 ›› Issue (6): 641-644.doi: 10.3969/j.issn.1006-9771.2018.06.004
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GONG Chao-yang, LIU Kai-xin, XIANG Gao, ZHANG Hai-hong
Received:2018-04-16
Revised:2018-05-21
Published:2018-06-25
Online:2018-06-28
Contact:
ZHANG Hai-hong. E-mail: zhanghaihong1968@sina.com
CLC Number:
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.
| [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. |
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