ArticleJournal of molecular neuroscience : MN2017
Inhibition of GSK-3β Activation Protects SD Rat Retina Against N-Methyl-N-Nitrosourea-Induced Degeneration by Modulating the Wnt/β-Catenin Signaling Pathway.
Article in Journal of molecular neuroscience : MN, 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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9 citing papers in PubMed, 15 citations in OpenAlex.
- Neuroprotective effect of ciclopirox olamine in retinal ischemia/reperfusion injury.BMC molecular and cell biology · 2024Article
- Pregabalin Mediates Retinal Ganglion Cell Survival From Retinal Ischemia/Reperfusion Injury Via the Akt/GSK3β/β-Catenin Signaling Pathway.Investigative ophthalmology & visual science · 2022Article
- GSK3 Is a Central Player in Retinal Degenerative Diseases but a Challenging Therapeutic Target.Cells · 2022Review
- Microarray-based gene expression analysis combined with laser capture microdissection is beneficial in investigating the modes of action of ocular toxicity.Journal of toxicologic pathology · 2022Article
- The neuroprotective role of Wnt signaling in the retina.Neural regeneration research · 2021Article
- Intraductal administration of N-methyl-N-nitrosourea as a novel rodent mammary tumor model.Annals of translational medicine · 2021Article
- Glycogen synthase kinase-3β inhibitor SB216763 promotes DNA repair in ischemic retinal neurons.Neural regeneration research · 2021Article
- Article
- Chronic noise exposure exacerbates AD-like neuropathology in SAMP8 mice in relation to Wnt signaling in the PFC and hippocampus.Scientific reports · 2018Article
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Retinal degenerative diseases are characterized by photoreceptor cell loss. Photoreceptor cell loss leading to retinal degeneration can be induced by N-methyl-N-nitrosourea (MNU), which was widely used to mimic the pathology. However, the mechanism by which MNU induces photoreceptor cell loss is still largely unknown. The purpose of the present study was to investigate whether phosphorylation of glycogen synthase kinase-3β (p-GSK-3β) is a potent mediator of MNU-induced retinal degeneration and how p-GSK-3β affects the process. MNU-induced photoreceptor cell loss was evaluated in Sprague-Dawley (SD) rat retinas. GSK-3β and Akt expression levels did not change during MNU-induced retinal degeneration but the phosphorylation of GSK-3β and Akt was decreased by MNU treatment. Lithium chloride (LiCl), which increases p-GSK-3β level and active-β-catenin level, reversed retinal degeneration induced by MNU treatment. These results suggest that GSK-3β activation is closely related to photoreceptor cell loss and that the application of the GSK-3β inhibitor LiCl could activate Wnt/β-catenin signaling pathway and reduce photoreceptor cell loss induced by MNU. Our findings indicate that inhibition of GSK-3β activation may be a potential therapeutic target for retinal degeneration induced by photoreceptor cell loss.
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