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首页> 外文期刊>Neuron >Thrombospondin-1 Mediates Axon Regeneration in Retinal Ganglion Cells
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Thrombospondin-1 Mediates Axon Regeneration in Retinal Ganglion Cells

机译：血压素蛋白-1介导视网膜神经节细胞中的轴突再生

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摘要

Neuronal subtypes show diverse injury responses, but the molecular underpinnings remain elusive. Using transgenic mice that allow reliable visualization of axonal fate, we demonstrate that intrinsically photo-sensitive retinal ganglion cells (ipRGCs) are both resilient to cell death and highly regenerative. Using RNA sequencing (RNA-seq), we show genes that are differentially expressed in ipRGCs and that associate with their survival and axon regeneration. Strikingly, thrombospondin-1 (Thbs1) ranked as the most differentially expressed gene, along with the well-documented injury-response genes Atf3 and Jun. THBS1 knockdown in RGCs eliminated axon regeneration. Conversely, RGC overexpression of THBS1 enhanced regeneration in both ipRGCs and non-ipRGCs, an effect that was dependent on syndecan- 1, a known THBS1-binding protein. All structural domains of the THBS1 were not equally effective; the trimerization and C-terminal domains promoted regeneration, while the THBS type-1 repeats were dispensable. Our results identify cell-type-specific induction of Thbs1 as a novel gene conferring high regenerative capacity.
机译：神经元亚型显示不同的伤害反应，但分子下限仍然难以捉摸。使用允许可靠的轴突命运可视化的转基因小鼠，我们证明了本质上的光敏视网膜神经节细胞（IPRGCs）既有弹性对细胞死亡和高再生。使用RNA测序（RNA-SEQ），我们显示在IPRGCS中差异表达的基因，并且与其存活和轴突再生相关联。尖锐的血压素-1（THBS1）作为最差异表达的基因排名，以及良好记录的损伤 - 反应基因ATF3和Jun。在RGCS中敲低轴突再生。相反，RGC过表达THBS1增强了IPRGC和非IPRGC的再生，一种依赖于Syndecan-1的效果，即已知的THBS1结合蛋白。 THBS1的所有结构域都没有同样有效;三聚化和C末端结构域促进再生，而THB型重复是可分配的。我们的结果鉴定了THBS1的细胞型特异性诱导作为赋予高再生能力的新基因。

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  • 来源
    《Neuron》 |2019年第4期|共23页
  • 作者

    Bray Eric R.; Yungher Benjamin J.; Levay Konstantin; Ribeiro Marcio; Dvoryanchikov Gennady; Ayupe Ana C.; Thakor Kinjal; Marks Victoria; Randolph Michael; Danzi Matt C.; Schmidt Tiffany M.; Chaudhari Nirupa; Lemmon Vance P.; Hattar Samer; Park Kevin K.;

  • 作者单位

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Physiol &

    Biophys Dept Otolaryngol Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Northwestern Univ Dept Neurobiol Evanston IL USA;

    Univ Miami Dept Physiol &

    Biophys Dept Otolaryngol Miller Sch Med Miami FL 33136 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

    Johns Hopkins Univ Dept Biol Baltimore MD 21218 USA;

    Univ Miami Dept Neurol Surg Miami Project Cure Paralysis Miller Sch Med Miami FL 33136 USA;

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  • 正文语种 eng
  • 中图分类 神经病学;
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