Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
批准号:
10629275
负责人:
Feliks Ephraim Trakhtenberg
金额:
$41.0万
依托单位国家:
美国
项目类别:
财政年份:
2019
资助国家:
美国
项目状态:
已结题
起止时间:
2019-06-01 至 2024-09-30
关键词:
AcuteAdultAffectAlgorithmsAnatomyAnimal ModelAxonBioinformaticsBiologicalBiological AssayBirthBlindnessBrainCell MaturationCellular biologyCentral Nervous SystemClinicDendritesDevelopmentEmbryoEyeFailureGenesGlaucomaGoalsGrowthInjuryIschemiaIschemic Optic NeuropathyKnowledgeMammalsMediatingMessenger RNAMethyl-CpG-Binding Protein 2MicroRNAsModelingMolecularMorphologyMouse StrainsMusNatural regenerationNerve CrushNeuronsOncogenicOptic NerveOptic Nerve InjuriesOptic tract structurePathway interactionsPeripheralPhasePlayProcessQuantitative Reverse Transcriptase PCRRNARecovery of FunctionRegenerative capacityResearchRetinaRetinal Ganglion CellsReview LiteratureRoleSmall RNASynaptic plasticityTestingTimeTranslationsTumor Suppressor ProteinsUntranslated RNAVisionVisualaxon growthaxon injuryaxon regenerationcandidate selectiondifferential expressionexperimental studyimprovedin vivoknock-downmature animalmouse modelneurite growthnovelnovel strategiesoptic nerve disorderoverexpressionperipheral nerve regenerationpiRNApostnatalpostsynapticpresynapticprospectiveregeneration potentialregenerativereinnervationrepairedresponseretinal stimulationside effectsmall hairpin RNAtranscriptome sequencingvector
中文摘要
项目摘要
视网膜神经节细胞通过视神经中的轴突将信息从眼睛传递到大脑,并
视神经束。视网膜神经节细胞轴突生长的分子机制尚不清楚,
成年视网膜神经节细胞不能自发再生受损的轴突,从而导致视力丧失。
与视神经损伤和视神经疾病有关。我们的目标是研究一种新的方法来
刺激视网膜神经节细胞通过视神经再生轴突的固有能力
视觉反应。我们将利用已建立的动物模型来研究小的非编码RNA的作用
在调节视网膜神经节细胞成熟和轴突生长能力的发育丧失方面,并检测其
有可能再生受损的视神经。我们还将调查通过哪些分子途径
已识别的小分子非编码RNA调节轴突生长。此外,我们将调查这些因素所起的作用
小分子非编码RNA在视网膜发育过程中视网膜神经节细胞树突的树枝状分布。我们预计
这些研究将促进我们对小的非编码RNA在视网膜神经节中所起作用的理解
细胞生物学,以及潜在地导致用于恢复简单视觉的新方法的发展
视神经损伤后的功能。
英文摘要
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.
期刊论文(12)
专著(0)
科研奖励(0)
会议论文
登录
查看更多内容
Pten inhibition dedifferentiates long-distance axon-regenerating intrinsically photosensitive retinal ganglion cells and upregulates mitochondria-associated Dynlt1a and Lars2.
Pten 抑制使长距离轴突再生的本质光敏视网膜神经节细胞去分化,并上调线粒体相关的 Dynlt1a 和 Lars2。
DOI:
10.1242/dev.201644
发表时间:
2023-04-15
期刊:
Development (Cambridge, England)
影响因子:
--
作者:
[]
通讯作者:
DOI:
10.1016/j.neulet.2021.136260
发表时间:
2021-11-20
期刊:
Neuroscience letters
影响因子:
2.5
作者:
[Lukomska A, Kim J, Rheaume BA, Xing J, Hoyt A, Lecky E, Steidl T, Trakhtenberg EF]
通讯作者:
Trakhtenberg EF
Post-injury born oligodendrocytes incorporate into the glial scar and contribute to the inhibition of axon regeneration.
损伤后产生的少突胶质细胞融入神经胶质疤痕并有助于抑制轴突再生。
DOI:
10.1242/dev.201311
发表时间:
2023-04-15
期刊:
Development (Cambridge, England)
影响因子:
--
作者:
[]
通讯作者:
DOI:
10.4103/1673-5374.380883
发表时间:
2024-03
期刊:
Neural regeneration research
影响因子:
6.1
作者:
[Trakhtenberg EF]
通讯作者:
Trakhtenberg EF
Experimental gene expression of developmentally downregulated Crmp1, Crmp4, and Crmp5 promotes axon regeneration and retinal ganglion cell survival after optic nerve injury.
发育下调 Crmp1、Crmp4 和 Crmp5 的实验基因表达可促进视神经损伤后轴突再生和视网膜神经节细胞存活。
DOI:
10.1016/j.brainres.2023.148368
发表时间:
2023
期刊:
Brain research
影响因子:
2.9
作者:
[Lukomska,Agnieszka, Theune,WilliamC, Xing,Jian, Frost,MatthewP, Damania,Ashiti, Gupta,Mahit, Trakhtenberg,EphraimF]
通讯作者:
Trakhtenberg,EphraimF
Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
-
批准号:10404950
-
项目类别:
-
资助金额:$39.77万
-
财政年份:2019
-
负责人:Feliks Ephraim Trakhtenberg
-
依托单位:
Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
-
批准号:10176509
-
项目类别:
-
资助金额:$39.77万
-
财政年份:2019
-
负责人:Feliks Ephraim Trakhtenberg
-
依托单位:
Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
-
批准号:9762351
-
项目类别:
-
资助金额:$40.97万
-
财政年份:2019
-
负责人:Feliks Ephraim Trakhtenberg
-
依托单位:
Small non-coding RNAs regulate retinal ganglion cell maturation and the developmental loss of intrinsic axon growth capacity
-
批准号:10004833
-
项目类别:
-
资助金额:$3.99万
-
财政年份:2019
-
负责人:Feliks Ephraim Trakhtenberg
-
依托单位:
海外基金