ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2014
Gap junction-mediated death of retinal neurons is connexin and insult specific: a potential target for neuroprotection.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 41 papers.
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41 citing papers in PubMed, 70 citations in OpenAlex.
- High Activity of Hemichannels Permeable to Calcium Ions Leads to ROS Generation and Reduced Cell Viability.International journal of molecular sciences · 2026Article
- Gap junction protein connexin 36 proteostatic mechanisms in photoreceptor cells subjected to excitotoxic stress.Acta biochimica Polonica · 2026Article
- The Role of Connexin 36 Gap Junctions in Retinal Ganglion Cell Death After Corneal Alkali Burns.Investigative ophthalmology & visual science · 2025Article
- The structure, function, and distribution of gap junctions in the retina: Life cycle in health and disease.Journal of cell communication and signaling · 2025Review
- Protector Role of Cx30.2 in Pancreatic β-Cell against Glucotoxicity-Induced Apoptosis.Biology · 2024Article
- Neuroprotective gap-junction-mediated bystander transformations in the adult zebrafish spinal cord after injury.Nature communications · 2024Article
- Sustained Extracellular Electrical Stimulation Modulates the Permeability of Gap Junctions inInternational journal of molecular sciences · 2024Article
- Evaluation of the neuroprotective efficacy of the gramine derivative ITH12657 against NMDA-induced excitotoxicity in the rat retina.Frontiers in neuroanatomy · 2024Article
- The Effect of Temperature on the Embryo Development of CephalopodInternational journal of molecular sciences · 2023Article
- Article
- Biotin-cGMP and -cAMP are able to permeate through the gap junctions of some amacrine cells in the mouse retina despite their large size.Frontiers in ophthalmology · 2023Article
- GAP junctions: multifaceted regulators of neuronal differentiation.Tissue barriers · 2022Article
- Gap Junctional Coupling Between Retinal Astrocytes Exacerbates Neuronal Damage in Ischemia-Reperfusion Injury.Investigative ophthalmology & visual science · 2021Article
- The role of gap junctions in cell death and neuromodulation in the retina.Neural regeneration research · 2021Review
- AXL kinase-mediated astrocytic phagocytosis modulates outcomes of traumatic brain injury.Journal of neuroinflammation · 2021Article
- Neuroprotection of the Inner Retina Also Prevents Secondary Outer Retinal Pathology in a Mouse Model of Glaucoma.Investigative ophthalmology & visual science · 2021Article
- PTEN Expression Regulates Gap Junction Connectivity in the Retina.Frontiers in neuroanatomy · 2021Article
- Retinal ganglion cell interactions shape the developing mammalian visual system.Development (Cambridge, England) · 2020Review
- Systemic Administration of an Apelin Receptor Agonist Prevents NMDA-Induced Loss of Retinal Neuronal Cells in Mice.Neurochemical research · 2020Article
- Role of Connexins 30, 36, and 43 in Brain Tumors, Neurodegenerative Diseases, and Neuroprotection.Cells · 2020Review
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Authors and funding
8 authors at 3 institutions in 1 country.
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Abstract
Secondary cell death via gap junctions (GJs) plays a role in the propagation of neuronal loss under a number of degenerative disorders. Here, we examined the role of GJs in neuronal death in the retina, which has arguably the most diverse expression of GJs in the CNS. Initially, we induced apoptotic death by injecting single retinal ganglion cells and glia with cytochrome C and found that this resulted in the loss of neighboring cells to which they were coupled via GJs. We next found that pharmacological blockade of GJs eradicated nearly all amacrine cell loss and reduced retinal ganglion cell loss by ∼70% after induction of either excitotoxic or ischemic insult conditions. These data indicate that the GJ-mediated secondary cell death was responsible for the death of most cells. Whereas genetic deletion of the GJ subunit Cx36 increased cell survivability by ∼50% under excitotoxic condition, cell loss in Cx45 knock-out mouse retinas was similar to that seen in wild-type mice. In contrast, ablation of Cx45 reduced neuronal loss by ∼50% under ischemic insult, but ablation of Cx36 offered no protection. Immunolabeling of the connexins showed differential changes in protein expression consistent with their differing roles in propagating death signals under the two insults. These data indicate that secondary cell death is mediated by different cohorts of GJs dependent on the connexins they express and the type of initial insult. Our results suggest that targeting specific connexins offers a novel therapeutic strategy to reduce progressive cell loss under different neurodegenerative conditions.
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