Neuritin 1 promotes retinal ganglion cell survival and axonal regeneration following optic nerve crush

Sharma, Tasneem Putliwala; Liu, Yang; Wordinger, Robert J.; Pang, Iok‐Hou; Clark, Abbot F.

doi:10.1038/cddis.2015.22

Cited by 46 publications

(34 citation statements)

References 76 publications

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“…Neuritin overexpression induces the recovery of crushed optic nerve in mouse (Sharma et al, 2015). We recently showed that recombinant Neuritin protects neurons against apoptosis following spinal cord injury (Gao et al, 2016).…”

Section: Introductionmentioning

confidence: 99%

Recombinant hNeuritin Promotes Structural and Functional Recovery of Sciatic Nerve Injury in Rats

Wang

Shan

et al. 2016

Front. Neurosci.

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Neuritin is a new neurotropic factor implicated in nervous system development and plasticity. Studies have shown that Neuritin is upregulated in injured nerves, suggesting that it is involved in nerve repair. To test this hypothesis, we investigated whether recombinant human Neuritin could restore nerve structure and function in a rat model of sciatic nerve injury. Neuritin treatment had a dose-dependent effect on functional recovery 4 weeks after injury, as determined by the walking-track test. Similar trends were observed for gastrocnemius muscular strength and nerve conduction velocity. Additionally, sciatic nerve fiber density and organization as well as degree of remyelination were increased, while growth-associated protein 43 and neurofilament 200 expression was upregulated upon treatment with Neuritin. These findings demonstrate that Neuritin stimulates nerve regeneration and functional recovery and thus promotes the repair of injured sciatic nerves.

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Section: Introductionmentioning

confidence: 99%

Recombinant hNeuritin Promotes Structural and Functional Recovery of Sciatic Nerve Injury in Rats

Wang

Shan

et al. 2016

Front. Neurosci.

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“…Notably, RGC markers had the highest downregulation fold changes, as for example, peripherin (-12.7x), neurofilament heavy, medium and light polypeptides (-11.4x, -11.8x and -6.8x, respectively), gamma synuclein (-10.8x), POU class 4 homeobox 2 (or Brn3A, -7.3x), Thy-1 cell surface antigen (-3.9x), synaptotagmin II (-2.4x), tubulin, beta 3 class III (-1.9x), internexin neuronal intermediate filament protein (-1.9x), alpha-internexin (-1.9x) and pannexin 2 (-1.89x). In addition, the retinal ganglion cell neurotrophic factor neuritin 1 [59] was also strongly down-regulated after ONC, with a -18.8x decrease when compared to controls ( Figure 2B). The EnrichR software, a tool to determine disease-enriched perturbations in the transcriptome that uses the GEO database, showed that among the down-regulated genes at 14 days after ONC, the top disease signature was "Glaucoma associated with systemic syndromes" (Table S4).…”

Section: Transcriptomic Alterations In Rat Retina After Optic Nerve Cmentioning

confidence: 92%

Optic Nerve Crush Activates the Genomic Fabrics of the Complement Cascade and Delta-Notch Signaling

Victorino¹,

Marra²,

Da³

et al. 2020

Preprint

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Glaucoma is a multifactorial neurodegenerative disease, characterized by degeneration of the retinal ganglion cells (RGCs). There has been little progress in developing efficient strategies for neuroprotection in glaucoma. We profiled the retina transcriptome of Lister Hooded rats at 2 weeks after optic nerve crush (ONC) and applied systems biology approaches to better understand the molecular mechanisms related with the retinal remodeling after induction of RGC degeneration. We observed a higher Relative Expression Variability after ONC. Gene expression stability was used as a measure of transcription control and disclosed a robust reduction in the number of very stably expressed genes. Enrichment analysis showed that Complement cascade and Notch signaling pathway were the main affected pathways after ONC. To expand our studies of these two pathways, we examined the coordination of gene expressions within each pathway and with the entire transcriptome. ONC increased the number of synergistically coordinated pairs of genes and the number of similar profiles. This study provided novel findings beyond the regulation of individual gene expression and disclosed changes in the control of expression by Complement cascade and Notch signaling functional pathways important for both RGC degeneration and remodeling of the retinal tissue after ONC.

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“…JAK/STAT, PI3K/Akt and MAPK/ERK. 49,50 This can be achieved for example by deletion of Krüppel-like family of transcription factors (KLF), 51 osteopontin, 52 phosphatase and tensin homolog (PTEN) 44,53,54 and/or suppressor of cytokine signaling 3 solution (SOCS3), 53,54 activation of the mechanistic target of rapamycin (mTOR) signaling pathway, 52,55 administration of Rho kinase (ROCK) inhibitors, 56 overexpression of glycogen synthase kinase 3 (GSK3), 57 c-myc, 58 neuritin-1, 59 or thrombospondin.-1 60 From recent studies, it is clear that multiple strategies that focus on both extrinsic and intrinsic factors should be combined to maximize axon outgrowth. 37,38,44,[61][62][63][64] For example, intraocular inflammation, cAMP, and PTEN deletion were found to act synergistically to augment regeneration.…”

Section: The Retinofugal System As a Model To Study Axonal Regenerationmentioning

confidence: 99%

Neuroinflammation and Optic Nerve Regeneration: Where Do We Stand in Elucidating Underlying Cellular and Molecular Players?

Andries

Groef

Moons

2019

Current Eye Research

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Neurodegenerative diseases and central nervous system (CNS) trauma are highly irreversible, in part because adult mammals lack a robust regenerative capacity. A multifactorial problem underlies the limited axonal regeneration potential. Strikingly, neuroinflammation seems able to induce axonal regrowth in the adult mammalian CNS. It is increasingly clear that both blood-borne and resident inflammatory cells as well as reactivated glial cells affect axonal regeneration. The scope of this review is to give a comprehensive overview of the knowledge that links inflammation (with a focus on the innate immune system) to axonal regeneration and to critically reflect on the controversy that still prevails about the cells, molecules and pathways that are dominating the scene. Also, a brief overview is given of what is already known about the crosstalk between and the heterogeneity of cell types that might play a role in axonal regeneration. Recent research indicates that inflammation-induced axonal regrowth is not solely driven by a single-cell population but probably relies on the crosstalk between multiple cell types and the strong regulation of these cell populations in time and space. Moreover, there is growing evidence that the different cell populations are highly heterogeneous and as such can react differently upon injury. This could explain the controversial results that have been obtained over the past years. The primary focus of this manuscript is the retinofugal system of adult mammals, however, when relevant, insights or examples of the spontaneous regenerating zebrafish model and spinal cord research are added.

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Neuritin 1 promotes retinal ganglion cell survival and axonal regeneration following optic nerve crush

Cited by 46 publications

References 76 publications

Recombinant hNeuritin Promotes Structural and Functional Recovery of Sciatic Nerve Injury in Rats

Recombinant hNeuritin Promotes Structural and Functional Recovery of Sciatic Nerve Injury in Rats

Optic Nerve Crush Activates the Genomic Fabrics of the Complement Cascade and Delta-Notch Signaling

Neuroinflammation and Optic Nerve Regeneration: Where Do We Stand in Elucidating Underlying Cellular and Molecular Players?

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