ArticleExperimental eye research2014
Acetylation: a lysine modification with neuroprotective effects in ischemic retinal degeneration.
Article in Experimental eye research, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 36 citations in OpenAlex.
- Deletion of myeloid HDAC3 promotes efferocytosis to ameliorate retinal ischemic injury.Journal of neuroinflammation · 2024Article
- The arginase 1/ornithine decarboxylase pathway suppresses HDAC3 to ameliorate the myeloid cell inflammatory response: implications for retinal ischemic injury.Cell death & disease · 2023Article
- Valproate reduces retinal ganglion cell apoptosis in rats after optic nerve crush.Neural regeneration research · 2023Article
- Roles of Histone Acetyltransferases and Deacetylases in the Retinal Development and Diseases.Molecular neurobiology · 2023Review
- Sphingomyelinases in retinas and optic nerve heads: Effects of ocular hypertension and ischemia.Experimental eye research · 2022Article
- Activation of Frizzled-7 attenuates blood-brain barrier disruption through Dvl/β-catenin/WISP1 signaling pathway after intracerebral hemorrhage in mice.Fluids and barriers of the CNS · 2021Article
- Reduction of Neuroinflammation by δ-Opioids Via STAT3-Dependent Pathway in Chronic Glaucoma Model.Frontiers in pharmacology · 2021Article
- Targeting HDAC3 in the DBA/2J spontaneous mouse model of glaucoma.Experimental eye research · 2020Article
- Histone Deacetylases Regulation by δ-Opioids in Human Optic Nerve Head Astrocytes.Investigative ophthalmology & visual science · 2020Article
- HDAC2 Regulates Glial Cell Activation in Ischemic Mouse Retina.International journal of molecular sciences · 2019Article
- The Histone Deacetylase Inhibitor AN7, Attenuates Choroidal Neovascularization in a Mouse Model.International journal of molecular sciences · 2019Article
- Proteomic determination of the lysine acetylome and phosphoproteome in the rat native inner medullary collecting duct.Physiological genomics · 2018Article
- Angiokine Wisp-1 is increased in myocardial infarction and regulates cardiac endothelial signaling.JCI insight · 2018Article
- Trichostatin A Inhibits Retinal Pigmented Epithelium Activation in an In Vitro Model of Proliferative Vitreoretinopathy.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2016Article
- Ischemic preconditioning, retinal neuroprotection and histone deacetylase activities.Experimental eye research · 2016Article
- Therapeutic Approaches to Histone Reprogramming in Retinal Degeneration.Advances in experimental medicine and biology · 2016Review
- Proteome Analysis of Renoprotection Mediated by a Novel Cyclic Helix B Peptide in Acute Kidney Injury.Scientific reports · 2015Article
- Pharmacological Modulation of Photoreceptor Outer Segment Degradation in a Human iPS Cell Model of Inherited Macular Degeneration.Molecular therapy : the journal of the American Society of Gene Therapy · 2015Article
- Histone Deacetylases Exert Class-Specific Roles in Conditioning the Brain and Heart Against Acute Ischemic Injury.Frontiers in neurology · 2015Review
- Acetylation preserves retinal ganglion cell structure and function in a chronic model of ocular hypertension.Investigative ophthalmology & visual science · 2014Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Neuroretinal ischemic injury contributes to several degenerative diseases in the eye and the resulting pathogenic processes involving a series of necrotic and apoptotic events. This study investigates the time and extent of changes in acetylation, and whether this influences function and survival of neuroretinal cells following injury. Studies evaluated the time course of changes in histone deacetylase (HDAC) activity, histone-H3 acetylation and caspase-3 activation levels as well as retinal morphology and function (electroretinography) following ischemia. In addition, the effect of two HDAC inhibitors, trichostatin-A and valproic acid were also investigated. In normal eyes, retinal ischemia produced a significant increase in HDAC activity within 2 h that was followed by a corresponding significant decrease in protein acetylation by 4 h. Activated caspase-3 levels were significantly elevated by 24 h. Treatment with HDAC inhibitors blocked the early decrease in protein acetylation and activation of caspase-3. Retinal immunohistochemistry demonstrated that systemic administration of trichostatin-A or valproic acid, resulted in hyperacetylation of all retinal layers after systemic treatment. In addition, HDAC inhibitors provided a significant functional and structural neuroprotection at seven days following injury relative to vehicle-treated eyes. These results provide evidence that increases in HDAC activity is an early event following retinal ischemia, and are accompanied by corresponding decreases in acetylation in advance of caspase-3 activation. In addition to preserving acetylation status, the administration of HDAC inhibitors suppressed caspase activation and provided structural and functional neuroprotection in model of ischemic retinal injury. Taken together these data provide evidence that decrease in retinal acetylation status is a central event in ischemic retinal injury, and the hyperacetylation induced by HDAC inhibition can provide acute neuroprotection.
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Registered trials
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