ArticleCell communication and signaling : CCS2024
Interleukin-4 protects retinal ganglion cells and promotes axon regeneration.
Article in Cell communication and signaling : CCS, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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7 citing papers in PubMed, 8 citations in OpenAlex.
- Annexin A1 as a Key Modulator of Inflammatory, Glial, and Angiogenic Signaling Pathways in Diabetic Retinopathy.Investigative ophthalmology & visual science · 2026Article
- Biopolymer-Conjugated Human C-Peptide Provides Sustained Neuroprotection and Preserves Axonal Transport in a Mouse Model of NMDA-Induced Retinal Degeneration via Antioxidative Mechanisms.Antioxidants (Basel, Switzerland) · 2026Article
- Strain-Dependent Differences in Baseline Retinal Immune Homeostasis: A Comparative Study of Albino and Pigmented Mice.Cellular and molecular neurobiology · 2026Article
- Multifunctional nanoplatforms for optic nerve regeneration integrating anti-inflammatory, epigenetic, and ionic mechanisms with emerging artificial intelligence technologies.Cell biology and toxicology · 2025Review
- AAV2.7m8 transduction of stage 2 human retinal organoids induces highly variable responses in innate and inflammatory gene expression and cytokine secretion.Experimental eye research · 2025Article
- Protocol for the purification and culture of primary retinal ganglion cells and development of common pathological models.Journal of molecular histology · 2025Article
- Deletion of Slc1a4 Suppresses Single Mauthner Cell Axon Regeneration In Vivo through Growth-Associated Protein 43.International journal of molecular sciences · 2024Article
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6 authors at 1 institution in 1 country.
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Abstract
backgroundThe preservation of retinal ganglion cells (RGCs) and the facilitation of axon regeneration are crucial considerations in the management of various vision-threatening disorders. Therefore, we investigate the efficacy of interleukin-4 (IL-4), a potential therapeutic agent, in promoting neuroprotection and axon regeneration of retinal ganglion cells (RGCs) as identified through whole transcriptome sequencing in an in vitro axon growth model.
methodsA low concentration of staurosporine (STS) was employed to induce in vitro axon growth. Whole transcriptome sequencing was utilized to identify key target factors involved in the molecular mechanism underlying axon growth. The efficacy of recombinant IL-4 protein on promoting RGC axon growth was validated through in vitro experiments. The protective effect of recombinant IL-4 protein on somas of RGCs was assessed using RBPMS-specific immunofluorescent staining in mouse models with optic nerve crush (ONC) and N-methyl-D-aspartic acid (NMDA) injury. The protective effect on RGC axons was evaluated by anterograde labeling of cholera toxin subunit B (CTB), while the promotion of RGC axon regeneration was assessed through both anterograde labeling of CTB and immunofluorescent staining for growth associated protein-43 (GAP43).
resultsWhole-transcriptome sequencing of staurosporine-treated 661 W cells revealed a significant upregulation in intracellular IL-4 transcription levels during the process of axon regeneration. In vitro experiments demonstrated that recombinant IL-4 protein effectively stimulated axon outgrowth. Subsequent immunostaining with RBPMS revealed a significantly higher survival rate of RGCs in the rIL-4 group compared to the vehicle group in both NMDA and ONC injury models. Axonal tracing with CTB confirmed that recombinant IL-4 protein preserved long-distance projection of RGC axons, and there was a notably higher number of surviving axons in the rIL-4 group compared to the vehicle group following NMDA-induced injury. Moreover, intravitreal delivery of recombinant IL-4 protein substantially facilitated RGC axon regeneration after ONC injury.
conclusionThe recombinant IL-4 protein exhibits the potential to enhance the survival rate of RGCs, protect RGC axons against NMDA-induced injury, and facilitate axon regeneration following ONC. This study provides an experimental foundation for further investigation and development of therapeutic agents aimed at protecting the optic nerve and promoting axon regeneration.
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