Department of Ophthalmology, Bascom Palmer Eye Institute, University of Miami Miller School of Medicine, 1638 NW 10th Ave, Miami, FL, 33136, USA.
Department of Microbiology and Immunology, University of Miami Miller School of Medicine, Miami, FL, 33136, USA.
Sci Rep. 2024 Nov 9;14(1):27412. doi: 10.1038/s41598-024-79296-0.
Optic nerve (ON) injury causes blindness in adult mammals as their retinal ganglion cells (RGCs) cannot regenerate axons. However, amphibian RGC axons do not experience the same regenerative failure. Studying the regeneration process of the ON in amphibians holds profound implications for regenerative medicine and human health. Using transgenic tadpoles and laser micro-optics, we developed a reproducible ON transection and regeneration model. Through microscopy of axon dynamics, functional testing to assess visual pathway recovery, TUNEL cell death and EdU cell proliferation assays, and RNA-seq of the retina and optic nerve, we characterized the optic nerve injury response and subsequent recovery. Our model suggests no chemoattractant gradient exists early in regeneration, with defasciculated axons sprouting in random directions from the globe-proximal cut end. Once individual axons reach the appropriate targets in the brain, their tract is reinforced by other regenerating axons, restoring normal ON morphology. Thus, guidance cues or scaffolding from brain-innervating axons likely support later stages of regeneration. After 14 days, the regenerated ON is morphologically indistinguishable from the naïve ON, and visual function is restored. We found no evidence of RGC death or new RGC formation in the model, suggesting that ON regeneration involves remodeling of injured axons of pre-existing RGCs.
视神经(ON)损伤会导致成年哺乳动物失明,因为它们的视网膜神经节细胞(RGC)无法再生轴突。然而,两栖类 RGC 轴突不会经历同样的再生失败。研究两栖类 ON 的再生过程对再生医学和人类健康具有深远的意义。我们使用转基因蝌蚪和激光微光学技术,开发了一种可重复的 ON 横断和再生模型。通过轴突动力学的显微镜观察、评估视觉通路恢复的功能测试、TUNEL 细胞死亡和 EdU 细胞增殖测定,以及视网膜和视神经的 RNA-seq,我们描述了视神经损伤反应和随后的恢复过程。我们的模型表明,在再生早期不存在趋化因子梯度,从球体近端切断端发散的解聚轴突随机发芽。一旦单个轴突到达大脑中的适当靶标,它们的轨迹就会被其他再生轴突加强,恢复正常的 ON 形态。因此,来自脑支配轴突的导向线索或支架可能支持再生的后期阶段。14 天后,再生的 ON 在形态上与未受伤的 ON 无法区分,并且视觉功能得到恢复。我们在该模型中没有发现 RGC 死亡或新的 RGC 形成的证据,这表明 ON 再生涉及受损的 RGC 轴突的重塑。