ArticleMolecular vision2017
Epigenetic intervention with a BET inhibitor ameliorates acute retinal ganglion cell death in mice.
Article in Molecular vision, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
What it found
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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
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- New Insights into the Role of Cellular Senescence and Its Therapeutic Implications in Ocular Diseases.Bioengineering (Basel, Switzerland) · 2025Review
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- Aging and aging-related diseases: from molecular mechanisms to interventions and treatments.Signal transduction and targeted therapy · 2022Review
- Epigenetic Regulation of Optic Nerve Development, Protection, and Repair.International journal of molecular sciences · 2022Review
- Activation of Apoptosis in a βB1-CTGF Transgenic Mouse Model.International journal of molecular sciences · 2021Article
- Cellular senescence in the aging retina and developments of senotherapies for age-related macular degeneration.Journal of neuroinflammation · 2021Review
- Treatment with JQ1, a BET bromodomain inhibitor, is selectively detrimental to R6/2 Huntington's disease mice.Human molecular genetics · 2020Article
- BET protein inhibition regulates cytokine production and promotes neuroprotection after spinal cord injury.Journal of neuroinflammation · 2019Article
- Toxicity of JQ1 in neuronal derivatives of human umbilical cord mesenchymal stem cells.Oncotarget · 2018Article
- Protective Effect of Hydrogen on Sodium Iodate-Induced Age-Related Macular Degeneration in Mice.Frontiers in aging neuroscience · 2018Article
- Potential independent action of sigma receptor ligands through inhibition of the Kv2.1 channel.Oncotarget · 2017Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
Abstract
purposeThe bromo and extraterminal (BET) epigenetic "reader" family is becoming an appealing new therapeutic target for several common diseases, yet little is known of its role in retinal neurodegeneration. We explored the potential of BET inhibition in the protection of retinal ganglion cells (RGCs).
methodsTo test the therapeutic effect of JQ1, an inhibitor highly selective for the BET family of proteins, we used an acute RGC damage model induced by N-methyl-D-aspartic acid (NMDA) excitotoxicity. Adult C57BL/6 mice received an intravitreal injection of NMDA with (or without) JQ1 in one eye and vehicle control in the contralateral eye; RGC loss was assessed on retinal sections and whole mounts. Gene expression and apoptosis were analyzed by quantitative real time (RT)-PCR and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL), respectively. For counting RGCs, immunostaining of the marker protein BRN3A was performed on whole mounts.
resultsNMDA treatment eliminated RGCs (day 7 and day 14 post injection) and diminished the expression (mRNAs) of RGC-selective genes, including
conclusionsIntravitreal injection of a BET inhibitor (JQ1) ameliorates NMDA-induced RGC death, revealing the RGC-protective potential of pharmacological blockage of the BET family. This new strategy of epigenetic intervention may be extended to other retinal degenerative conditions.
Indexed as
Identifiers
28356707PMC5360452W2760474850What OpenQuestion holds
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.