ArticleJournal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics2018
Targeting HDAC3 Activity with RGFP966 Protects Against Retinal Ganglion Cell Nuclear Atrophy and Apoptosis After Optic Nerve Injury.
Article in Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 45 citations in OpenAlex.
- Quantitative Analysis of Plasmid DNA Distribution and Transgene Expression Following Cell Squeezing.Annals of biomedical engineering · 2026Article
- Myeloid HDAC3 deletion protects against traumatic optic injury.Cell death discovery · 2026Article
- Retinoid X receptor agonist 9CDHRA mitigates retinal ganglion cell apoptosis and neuroinflammation in a mouse model of glaucoma.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2025Article
- Preservation of Murine Whole Eyes With Supplemented UW Cold Storage Solution: Anatomical Considerations.Translational vision science & technology · 2024Article
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury.Journal of neuroinflammation · 2024Article
- The role of HDAC3 in inflammation: mechanisms and therapeutic implications.Frontiers in immunology · 2024Review
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Molecular neurodegeneration · 2023Article
- BAX activation in mouse retinal ganglion cells occurs in two temporally and mechanistically distinct steps.Research square · 2023Article
- Roles of Histone Acetyltransferases and Deacetylases in the Retinal Development and Diseases.Molecular neurobiology · 2023Review
- Aging Effects on Optic Nerve Neurodegeneration.International journal of molecular sciences · 2023Review
- Epigenetic Regulation of Optic Nerve Development, Protection, and Repair.International journal of molecular sciences · 2022Review
- Inhibition of Epigenetic Modifiers LSD1 and HDAC1 Blocks Rod Photoreceptor Death in Mouse Models of Retinitis Pigmentosa.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2021Article
- Increased Susceptibility and Intrinsic Apoptotic Signaling in Neurons by Induced HDAC3 Expression.Investigative ophthalmology & visual science · 2021Article
- Genome-wide chromatin accessibility analyses provide a map for enhancing optic nerve regeneration.Scientific reports · 2021Article
- HDAC3 Downregulation Improves Cerebral Ischemic Injury via Regulation of the SDC1-Dependent JAK1/STAT3 Signaling Pathway Through miR-19a Upregulation.Molecular neurobiology · 2021Article
- Changes in Class I and IIb HDACs by δ-Opioid in Chronic Rat Glaucoma Model.Investigative ophthalmology & visual science · 2020Article
- Targeting HDAC3 in the DBA/2J spontaneous mouse model of glaucoma.Experimental eye research · 2020Article
- Dynamic Expression of HDAC3 in db/db Mouse RGCs and Its Relationship with Apoptosis and Autophagy.Journal of diabetes research · 2020Article
- HDAC3 Activity is Essential for Human Leukemic Cell Growth and the Expression of β-catenin, MYC, and WT1.Cancers · 2019Article
- Roles of mTOR Signaling in Tissue Regeneration.Cells · 2019Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
Abstract
purposeHDAC3 regulates nuclear atrophy as an early response to axonal injury in retinal ganglion cells (RGCs) following optic nerve crush (ONC). Since conditional knockout of Hdac3 prevents nuclear atrophy post ONC, HDAC3 selective inhibition with RGFP966 through localized and systemic dosing of RGFP966 is necessary for application to acute and chronic models of optic nerve injury.
methodsC57BL/6 mice were injected intravitreally with 1-10 μM RGFP966 immediately following ONC, and retinas were analyzed at 5, 7, and 14 days for metrics of nuclear atrophy and cell loss. Mice were similarly assessed after intraperitoneal (IP) injections with RGFP966 doses of 2-10 mg/kg, and eyes were harvested at 5, 14, and 28 days after ONC. H&E and BrdU staining were used to analyze toxicity to off-target tissues after 14 days of daily treatment with RGFP966.
resultsA single intravitreal injection of RGFP966 prevented histone deacetylation, heterochromatin formation, apoptosis, and DNA damage at 5 and 7 days post ONC. After IP injection, RGFP966 bioavailability in the retina reached peak concentration within 1 h after injection and then rapidly declined. A single IP injection of 2-10 mg/kg RGFP966, significantly prevented histone deacetylation. Repeated IP injections of 2 mg/kg RGFP966 over the course of 2 and 4 weeks post ONC prevented RGC loss. There were no significant toxic or antiproliferative effects to off-target tissues in mice treated daily for 14 days with RGFP966.
conclusionInhibition of HDAC3 activity with systemic dosing of RGFP966 prevents apoptosis-related histone deacetylation and attenuates RGC loss after acute optic nerve injury.
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Registered trials
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.