中国神经再生研究(英文版) ›› 2021, Vol. 16 ›› Issue (10): 2002-2003.doi: 10.4103/1673-5374.308094

• 观点:视神经损伤修复保护与再生 • 上一篇    下一篇

OTX2信号传导在视网膜功能障碍、变性和再生中的作用

  

  • 出版日期:2021-10-15 发布日期:2021-03-19

OTX2 signaling in retinal dysfunction, degeneration and regeneration

Kenneth. L. Moya*, Raoul Torero Ibad*   

  1. Centre for Interdisciplinary Research in Biology (CIRB), Collège de France, CNRS UMR 7241, INSERM U1050, Labex MemoLife, PSL Research University, Paris, France (Moya KL, Ibad RT)
    Univ. Lille, CNRS, UMR 8523 -PhLAM -Physique des Lasers Atomes et Molécules, F-59000 Lille, France (Ibad RT)
  • Online:2021-10-15 Published:2021-03-19
  • Contact: Kenneth. L. Moya, PhD, ken.moya@college-de-france.fr; Raoul Torero Ibad, PhD, raoul.torero@univ-lille.fr.
  • Supported by:
    We thank France Maloumian of the Collège de France (Paris, France) for graphic illustration.

    KLM is a coinventor for the use of OTX2 in eye disease and a cofounder of BrainEver.

    This work was supported by HOMEOSIGN: ERC-2013-AdG n°339379 and NeuroprOtx: ANR-16-CE16-0003-02.

摘要:

Neural Regen ResOTX2对视网膜神经元的神经保护作用

OTX2是一种同源蛋白转录因子,可以自主发挥细胞功能或在细胞间转移,并具有非细胞自主作用。除了其在发育过程中的重要作用外,这种蛋白质在发育的视网膜中的持续表达对正常生理学是必要的。OTX2在光感受器和双极细胞中表达,蛋白水平降低导致视网膜结构改变、视网膜色素上皮缺陷、神经元变性和视力丧失。OTX2在视网膜色素上皮中也有表达,这种蛋白在视网膜色素上皮中的再表达可以补偿整个视网膜中蛋白质的丢失,促进感光细胞的存活。OTX2的神经保护作用也延伸到成年视神经细胞,在这种情况下,这种蛋白质是非细胞自主的。干扰OTX2在视网膜中的非自主信号改变视网膜内部功能并导致视觉缺陷,强调了这种同源蛋白信号在正常生理中的重要性。OTX2对视网膜神经元的神经保护作用以及最近关于轴突再生的报道为视网膜退行性疾病,如年龄相关性黄斑变性和青光眼带来了新的治疗可能性。

相关观点文章在《中国神经再生研究(英文版)》杂志202110 月  10 期发表。


Abstract: The protein OTX2 in the retina is necessary for the maintenance of normal physiologic processes, and may be a promising therapeutic agent for some ophthalmic diseases. In this Perspective, we first shortly introduce the organization of the retina and the importance of OTX2 expression. We then present an example of reduced OTX2 activity in the developed retina associated with structural and functional consequences. We next show that homeoproteins can have neuroprotective functions. We finally review several clear examples of OTX2 non-cell autonomous activity in the retina and the effects of diminishing or providing extracellular OTX2.