Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity

小非编码 RNA 调节视网膜神经节细胞成熟和内在轴突生长能力的发育丧失

基本信息

批准号：
10176509
负责人：
Feliks Ephraim Trakhtenberg
金额：
$ 39.77万
依托单位：
UNIVERSITY OF CONNECTICUT SCH OF MED/DNT
依托单位国家：
美国
项目类别：
财政年份：
2019
资助国家：
美国
起止时间：
2019-06-01 至 2024-05-31
项目状态：
已结题

项目摘要

Project Summary The retinal ganglion cells convey information from the eye to the brain through their axons in the optic nerve and the optic tract. The molecular mechanisms of retinal ganglion cell axon growth are still poorly understood, and adult retinal ganglion cells do not spontaneously regenerate injured axons, contributing to the loss of vision associated with optic nerve trauma and optic neuropathies. Our goal is to investigate a novel approach for stimulating the retinal ganglion cells’ intrinsic capacity to regenerate axons through the optic nerve to restore visual responses. We will utilize established animal models for investigating the roles of small non-coding RNAs in regulating retinal ganglion cell maturation and the developmental loss of axon growth capacity, and test their potential for regenerating the injured optic nerve. We will also investigate through which molecular pathways the identified small non-coding RNAs regulate neurite growth. Furthermore, we will investigate the roles of these small non-coding RNAs in arborization of retinal ganglion cell dendrites during retinal development. We expect that these studies will advance our understanding of the roles the small non-coding RNAs play in retinal ganglion cell biology, as well as potentially lead to the development of novel approaches for restoring simple visual functions after optic nerve injury.

项目摘要视网膜神经节细胞通过视神经中的轴突从眼睛传达到大脑的信息，视线。残留神经节细胞轴突生长的分子机制仍然很了解，并且成年视网膜神经节细胞不会赞助再生受伤的轴突，导致视力丧失与视神经外伤和视神经病变有关。我们的目标是调查一种新颖的方法刺激视网膜神经节细胞通过视神经再生轴突的内在能力以恢复视觉响应。我们将利用既定的动物模型来研究小型非编码RNA的作用在控制视网膜神经节细胞的成熟和轴突生长能力的发育丧失时，并测试再生受伤的视神经的潜力。我们还将研究哪种分子途径鉴定出小的非编码RNA调节神经蛋白的生长。此外，我们将研究这些作用视网膜发育过程中视网膜神经节细胞树突的树木伪造中的小型非编码RNA。我们期望这些研究将提高我们对残留神经节中小型非编码RNA扮演的作用的理解细胞生物学，并有可能导致开发新的方法来恢复简单的视觉视神经损伤后的功能。