ArticleScientific reports2021
Effects of intravitreal injection of siRNA against caspase-2 on retinal and optic nerve degeneration in air blast induced ocular trauma.
Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 16 citations in OpenAlex.
- rAAV prostaglandin-based gene therapy lowers intraocular pressure and preserves optic nerve health in glaucomatous DBA/2J mice.bioRxiv : the preprint server for biology · 2026Article
- Review
- An improved method of transducing retinal ganglion cells using AAV via transpupillary injection in adult mouse eyes.Molecular vision · 2025Article
- Bi-allelic truncating variants in CASP2 underlie a neurodevelopmental disorder with lissencephaly.European journal of human genetics : EJHG · 2024Article
- Distribution and synaptic organization of substance P-like immunoreactive neurons in the mouse retina.Brain structure & function · 2023Article
- Optic nerve diseases and regeneration: How far are we from the promised land?Clinical & experimental ophthalmology · 2023Review
- Necroptosis plays a crucial role in the exacerbation of retinal injury after blunt ocular trauma.Neural regeneration research · 2023Article
- MicroRNA profile of extracellular vesicles released by Müller glial cells.Frontiers in cellular neuroscience · 2023Article
- Effect of Repeated Intravitreal Injections in Glaucoma Spectrum Diseases [Letter].Clinical ophthalmology (Auckland, N.Z.) · 2023Article
- Traumatic optic neuropathy: a review of current studies.Neurosurgical review · 2022Review
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Authors and funding
7 authors at 3 institutions in 2 countries.
Funding
Abstract
Ocular repeated air blast injuries occur from low overpressure blast wave exposure, which are often repeated and in quick succession. We have shown that caspase-2 caused the death of retinal ganglion cells (RGC) after blunt ocular trauma. Here, we investigated if caspase-2 also mediates RGC apoptosis in a mouse model of air blast induced indirect traumatic optic neuropathy (b-ITON). C57BL/6 mice were exposed to repeated blasts of overpressure air (3 × 2 × 15 psi) and intravitreal injections of siRNA against caspase-2 (siCASP2) or against a control enhanced green fluorescent protein (siEGFP) at either 5 h after the first 2 × 15 psi ("post-blast") or 48 h before the first blast exposure ("pre-blast") and repeated every 7 days. RGC counts were unaffected by the b-ITON or intravitreal injections, despite increased degenerating ON axons, even in siCASP2 "post-blast" injection groups. Degenerating ON axons remained at sham levels after b-ITON and intravitreal siCASP2 "pre-blast" injections, but with less degenerating axons in siCASP2 compared to siEGFP-treated eyes. Intravitreal injections "post-blast" caused greater vitreous inflammation, potentiated by siCASP2, with less in "pre-blast" injected eyes, which was abrogated by siCASP2. We conclude that intravitreal injection timing after ocular trauma induced variable retinal and ON pathology, undermining our candidate neuroprotective therapy, siCASP2.
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