Department of Neurological Surgery, Miami Project to Cure Paralysis, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Department of Physiology & Biophysics, Department of Otolaryngology, University of Miami Miller School of Medicine, Miami, FL 33136, USA.
Neuron. 2019 Aug 21;103(4):642-657.e7. doi: 10.1016/j.neuron.2019.05.044. Epub 2019 Jun 26.
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 photosensitive 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.
神经元亚型表现出不同的损伤反应,但分子基础仍难以捉摸。使用允许可靠观察轴突命运的转基因小鼠,我们证明内在光敏视网膜神经节细胞 (ipRGC) 既具有抗细胞死亡能力,又具有高度再生能力。通过 RNA 测序 (RNA-seq),我们展示了在 ipRGC 中差异表达的与它们的存活和轴突再生相关的基因。引人注目的是,血小板反应蛋白 1 (Thbs1) 与众所周知的损伤反应基因 Atf3 和 Jun 一起被列为差异表达最显著的基因。RGC 中的 THBS1 敲低消除了轴突再生。相反,RGC 中 THBS1 的过表达增强了 ipRGC 和非 ipRGC 的再生,这种效应依赖于已知与 THBS1 结合的蛋白 syndecan-1。THBS1 的所有结构域都不是同等有效的;三聚化和 C 末端结构域促进了再生,而 THBS 型 1 重复是可有可无的。我们的结果确定了 Thbs1 的细胞类型特异性诱导是赋予高再生能力的新基因。