ArticleScientific reports2017
Norrin protects optic nerve axons from degeneration in a mouse model of glaucoma.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
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Who cites it
9 citing papers in PubMed, 18 citations in OpenAlex.
- Leveraging Alzheimer's Disease Omics to Identify Pleiotropic Genes Contributing to Neurodegeneration in Primary Open-Angle Glaucoma.Molecular neurobiology · 2025Article
- The neuroprotective role of Wnt signaling in the retina.Neural regeneration research · 2021Article
- Norrin mediates tumor-promoting and -suppressive effects in glioblastoma via Notch and Wnt.The Journal of clinical investigation · 2020Article
- Norrin mediates opposing effects on tumor progression of glioblastoma stem cells.The Journal of clinical investigation · 2020Article
- Neuro-protection and neuro-regeneration of the optic nerve: recent advances and future directions.Current opinion in neurology · 2020Review
- Article
- Endogenous Wnt/β-catenin signaling in Müller cells protects retinal ganglion cells from excitotoxic damage.Molecular vision · 2020Article
- Dose-dependent regulation of horizontal cell fate by Onecut family of transcription factors.PloS one · 2020Article
- Recent advances in genetically modified animal models of glaucoma and their roles in drug repositioning.The British journal of ophthalmology · 2019Review
Corrections and comments
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Authors and funding
9 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Norrin is a secreted signaling molecule activating the Wnt/β-catenin pathway. Since Norrin protects retinal neurons from experimental acute injury, we were interested to learn if Norrin attenuates chronic damage of retinal ganglion cells (RGC) and their axons in a mouse model of glaucoma. Transgenic mice overexpressing Norrin in the retina (Pax6-Norrin) were generated and crossed with DBA/2J mice with hereditary glaucoma and optic nerve axonal degeneration. One-year old DBA/2J/Pax6-Norrin animals had significantly more surviving optic nerve axons than their DBA/2J littermates. The protective effect correlated with an increase in insulin-like growth factor (IGF)-1 mRNA and an enhanced Akt phosphorylation in DBA/2J/Pax6-Norrin mice. Both mouse strains developed an increase in intraocular pressure during the second half of the first year and marked degenerative changes in chamber angle, ciliary body and iris structure. The degenerations were slightly attenuated in the chamber angle of DBA/2J/Pax6-Norrin mice, which showed a β-catenin increase in the trabecular meshwork. We conclude that high levels of Norrin and the subsequent constitutive activation of Wnt/β-catenin signaling in RGC protect from glaucomatous axonal damage via IGF-1 causing increased activity of PI3K-Akt signaling. Our results identify components of a protective signaling network preventing degeneration of optic nerve axons in glaucoma.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.