ArticlePloS one2016
Astrocyte Structural and Molecular Response to Elevated Intraocular Pressure Occurs Rapidly and Precedes Axonal Tubulin Rearrangement within the Optic Nerve Head in a Rat Model.
Article in PloS one, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 51 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
51 citing papers in PubMed, 76 citations in OpenAlex.
- Compression injury regulates astrocyte morphology, metabolic function, and extracellular matrix modification in a 3D hydrogel.bioRxiv : the preprint server for biology · 2025Article
- Sustained Neurotrophic Factor Co-Treatment Enhances Donor and Host Retinal Ganglion Cell Survival in Mice.Translational vision science & technology · 2025Article
- Targeting Connexin 43 in Retinal Astrocytes Promotes Neuronal Survival in Glaucomatous Injury.Glia · 2025Article
- Targeting glial fibrillary acidic protein in glaucoma: a monoclonal antibody approach to modulate glial reactivity and neuroinflammation for neuroprotection.Journal of neuroinflammation · 2025Article
- A system for producing controlled elevation of intraocular pressure in awake Brown Norway rats.Experimental eye research · 2025Article
- Glial-mediated immune modulation in glaucomatous neurodegeneration: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
- Extracellular vesicles as emerging players in glaucoma: Mechanisms, biomarkers, and therapeutic targets.Vision research · 2025Review
- Controlled Elevation of Intraocular Pressure (CEI) Glaucoma Model in Rats.Methods in molecular biology (Clifton, N.J.) · 2025Article
- Mechanobiology in the eye.npj biological physics and mechanics · 2025Review
- Acute ocular hypertension in the living human eye: Model description and initial cellular responses to elevated intraocular pressure.Vision research · 2024Article
- Retinal Neurodegeneration in an Intraocular Pressure Fluctuation Rat Model.International journal of molecular sciences · 2024Article
- IOP and glaucoma damage: The essential role of optic nerve head and retinal mechanosensors.Progress in retinal and eye research · 2024Review
- Evaluation of the LDN-0060609 PERK Inhibitor as a Selective Treatment for Primary Open-Angle Glaucoma: An In Vitro Study on Human Retinal Astrocytes.International journal of molecular sciences · 2024Article
- Glaucoma: from pathogenic mechanisms to retinal glial cell response to damage.Frontiers in cellular neuroscience · 2024Review
- Comparison of the Biomechanics of the Mouse Astrocytic Lamina Cribrosa Between Glaucoma and Optic Nerve Crush Models.Investigative ophthalmology & visual science · 2023Article
- Retinal ganglion cell repopulation for vision restoration in optic neuropathy: a roadmap from the RReSTORe Consortium.Molecular neurodegeneration · 2023Review
- Astrocytes in the Optic Nerve Are Heterogeneous in Their Reactivity to Glaucomatous Injury.Cells · 2023Article
- Astrocyte polarization in glaucoma: a new opportunity.Neural regeneration research · 2022Review
- Microglia depletion exacerbates retinal ganglion cell loss in a mouse model of glaucoma.Experimental eye research · 2022Article
- Optic Nerve Head Myelin-Related Protein, GFAP, and Iba1 Alterations in Non-Human Primates With Early to Moderate Experimental Glaucoma.Investigative ophthalmology & visual science · 2022Article
Corrections and comments
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Authors and funding
10 authors at 1 institution in 1 country.
Funding
Abstract
Glaucomatous axon injury occurs at the level of the optic nerve head (ONH) in response to uncontrolled intraocular pressure (IOP). The temporal response of ONH astrocytes (glial cells responsible for axonal support) to elevated IOP remains unknown. Here, we evaluate the response of actin-based astrocyte extensions and integrin-based signaling within the ONH to 8 hours of IOP elevation in a rat model. IOP elevation of 60 mm Hg was achieved under isoflurane anesthesia using anterior chamber cannulation connected to a saline reservoir. ONH astrocytic extension orientation was significantly and regionally rearranged immediately after IOP elevation (inferior ONH, 43.2° ± 13.3° with respect to the anterior-posterior axis versus 84.1° ± 1.3° in controls, p<0.05), and re-orientated back to baseline orientation 1 day post IOP normalization. ONH axonal microtubule filament label intensity was significantly reduced 1 and 3 days post IOP normalization, and returned to control levels on day 5. Phosphorylated focal adhesion kinase (FAK) levels steadily decreased after IOP normalization, while levels of phosphorylated paxillin (a downstream target of FAK involved in focal adhesion dynamics) were significantly elevated 5 days post IOP normalization. The levels of phosphorylated cortactin (a downstream target of Src kinase involved in actin polymerization) were significantly elevated 1 and 3 days post IOP normalization and returned to control levels by day 5. No significant axon degeneration was noted by morphologic assessment up to 5 days post IOP normalization. Actin-based astrocyte structure and signaling within the ONH are significantly altered within hours after IOP elevation and prior to axonal cytoskeletal rearrangement, producing some responses that recover rapidly and others that persist for days despite IOP normalization.
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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.