ArticleActa biomaterialia2025
Co-delivery of neurotrophic factors and a zinc chelator substantially increases retinal ganglion cell survival and axon protection in the optic nerve crush model.
Article in Acta biomaterialia, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Metal-dependent regulated cell death: Molecular architecture and translational frontiers.iMeta · 2026Review
- Self-amplifying RNA therapy encoding CNTF with disulfiram co-delivery promotes optic nerve repair through microglial pyroptosis inhibition and RGC axonal regeneration.Journal of nanobiotechnology · 2026Article
- Synaptic control of retinal ganglion cell survival and axon regeneration.Molecular neurodegeneration · 2026Review
- Multifunctional nanoplatforms for optic nerve regeneration integrating anti-inflammatory, epigenetic, and ionic mechanisms with emerging artificial intelligence technologies.Cell biology and toxicology · 2025Review
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Abstract
Traumatic optic neuropathies lead to retinal ganglion cell (RGC) death and axonal degeneration, primarily due to disrupted neurotrophic factor (NTF) supply from the brain and a neurotoxic cascade, potentially mediated by elevated retinal Zn²⁺ levels. Ciliary neurotrophic factor (CNTF) and brain-derived neurotrophic factor (BDNF) are two major NTFs known to support RGC survival and axon protection. Dipicolylamine (DPA), a Zn²⁺ chelator with high selectivity and affinity, offers a strategy to reduce excess Zn²⁺. To achieve sustained NTF delivery and Zn²⁺ reduction, we developed sulfonated poly(serinol hexamethylene urea) nanoparticles (S-PSHU NPs) co-loaded with CNTF, BDNF, and DPA. In vitro release studies demonstrated sustained release of CNTF and BDNF for up to 8 weeks and DPA for up to 4 weeks. In a rat optic nerve crush (ONC) model, DPA-loaded S-PSHU NPs showed dose-dependent elimination of retinal Zn²⁺. Additionally, in primary RGC culture, RGC activity and axon growth correlated with CNTF and BDNF dosage. In vivo, NTF-DPA-loaded S-PSHU NPs significantly enhanced RGC survival and axon protection post-ONC, as evidenced by cholera toxin subunit B (CTB)-labeled axons in the central visual centers of the brain, including the suprachiasmatic nucleus, lateral geniculate nucleus, and superior colliculus. STATEMENT OF SIGNIFICANCE: • Co-delivery of neurotrophic factors (NTFs: CNTF and BDNF) and a zinc chelator (dipicolylamine, DPA) promotes retinal ganglion cell (RGC) axon survival and protection. • Sustained release of NTFs for up to 8 weeks and DPA for up to 4 weeks. • DPA-loaded nanoparticles effectively eliminate excess retinal zinc after optic nerve injury. • NTF-DPA-loaded nanoparticles significantly improve RGC survival and axon protection in a rat optic nerve crush model.
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