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少突胶质细胞和脊髓损伤 被引量:2

Oligodendrocyte and Spinal Cord Injury
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摘要 脊髓损伤(SCI)的过程中伴随着大量少突胶质细胞(OLs)的死亡,而OLs的死亡直接导致有髓神经纤维失去正常的电传导作用,引起脊髓的上下传导功能减弱甚至丧失,最终导致机体的感觉及运动功能损伤。因此本综述归纳了SCI后影响OLs死亡的各种微环境,并简述了OLs再生和髓鞘再生在SCI修复中的重要作用。最后针对影响OLs死亡和再生的各种因素,对SCI的治疗方式进行了分类总结,并对OLs在SCI治疗中的应用前景作了展望。 Spinal cord injury (SCI) is frequently eompanied by necrosis and apoptosis of oligodendrocytes(OLs), which contributes to demyelination of myelinated nerve fibers and their electrophysiological defects. This pathological demyelination often results in sensory or motor deficits. Here, we first focus on the mieroenvironment changes after SCI that cause OLs' death, then discuss the major mechanism of endogenous oligodendrocytogenesis and axonal remyelination, and finally summarize current therapies targeting OLs protection and replacement.
出处 《生物医学工程学杂志》 CAS CSCD 北大核心 2012年第6期1226-1229,共4页 Journal of Biomedical Engineering
关键词 脊髓损伤 少突胶质细胞 髓鞘再生 治疗 Spinal cord injury (SCI) Oligodendrocytes (OLs) Remyelination Therapy
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参考文献35

  • 1JAKOVCEVSKI I, FILIPOVIC R, MO Z C, et al. Oligoden- droeyte development and the onset of myelination in the hu- man fetal brain[J]. Front Neuroanat, 2009, 3:5.
  • 2MATIS G K, BIRBILIS T A. Erythropoietin in spinal cord injury[J]. Eur Spine J, 2009, 18(3): 314-323.
  • 3RASOULI A, BHATIA N, DINH P, et al. Resection of glial scar following spinal cord injury[J].J Orthop Res, 2009, 27 (7) : 931-936.
  • 4KADOYA K, TSUKADA S, LU P, et al. Combined intrinsic and extrinsic neuronal mechanisms facilitate bridging axonal regeneration one year after spinal cord injury[J]. Neuron, 2009, 64(2) : 165-172.
  • 5BEATTIE M S, FERGUSON A R, BRESNAHAN J C. AMPA-receptor trafficking and injury-induced cell death[J]. EurJ Neurosci, 2010, 32(2):290-297.
  • 6GUDZ T I, KOMURO H, MACKLIN W B. Glutamate stim- ulates oligodendrocyte progenitor migration mediated via an alphav integrin/myelin proteolipid protein complex [J]. J Neurosci, 2006, 26(9): 2458-2466.
  • 7DOMERCQ M, PEREZ-SAMARTIN A, APARICIO D, et al. P2X7 receptors mediate ischemic damage to oligodendro- cytes[J]. Glia, 2010, 58(6): 730-740.
  • 8TIAN D S, LIU J L, XIE M J, et al. Tamoxifen attenuates inflammatory-mediated damage and improves functional out- come after spinal cord injury in rats[J]. J Neurochem, 2009, 109(6) :1658-1667.
  • 9BECK K D, NGUYEN H X, GALVAN M D, et al. Quanti- tative analysis of cellular inflammation after traumatic spinal cord injury: evidence for a multiphasic inflammatory response in th e acute to chronic environment[J]. Brain, 2010, 133 (2) : 433-447.
  • 10WANG L, HU B, WONG W M, et al. Glial and axonal re- sponses in areas of Wallerian degeneration of the corticospinaland dorsal ascending tracts after spinal cord dorsal funiculoto- my[J]. Neuropathology, 2009, 29(3): 230-241.

二级参考文献9

  • 1Nicolay DJ, Doucette JR, Nazarali AJ. Transcriptional control of oligodendrogenesis. Glia, 2007, 55 : 1287-1299.
  • 2Fu H, Qi Y, Tan M, et al. Dual origin of spinal oligodendrocyte progenitors and evidence for the cooperative role of Olig2 and Nkx2.2 in the control of oligodendrocyte differentiation. Development,2002, 129:681 -693.
  • 3Meyer NP, Roelink H. The amino-terminal region of Gli3 antagonizes the Shh response and acts in dorsoventral fate specification in the developing spinal cord. Dev Biol, 2003, 257 : 343 - 355.
  • 4Zhou Q, Anderson DJ. The bHLH transcription factors OLIG2 and OLIG1 couple neuronal and gial subtype specification. Cell, 2002, 109 : 61 -73.
  • 5Zhou Q, Anderson DJ. The bHLH transcription factors OLIG2 and OLIG1 couple neuronal and glial subtype specification. Cell, 2002, 109 : 61 -73.
  • 6Xin M, Yue T, Ma Z, et al. Myelinogenesis and axonal recognition by oligodendrocytes in brain are uncoupled in Olig- 1-null mice. J Neurosci, 2005, 25 : 1354-1365.
  • 7Wang S-Z, Dulin J, Wu H, et al. An oligodendrocyte-specific zinc-finger transcription regulator cooperates with Olig2 to promote oligodendrocyte differentiation. Development, 2006, 133:3389-3398.
  • 8Li H, Lu Y, Simth HK, et al. Oligl and Sox10 interact synergistically to drive myelin basic protein transcription in oligodendrocytes. J Neurosci, 2007, 27 : 14375-14382.
  • 9Gokhan S, Marin-Husstege M, Yung SY, et al. Combinatorial profiles of oligodendrocyte-selective classes of transcriptional regulators differentially modulate myelin basic protein gene expression. J Neurosci, 2005, 25 : 8311 -8321.

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