ArticleJournal of neuroscience research2017
Sustained activation of ERK1/2 MAPK in Schwann cells causes corneal neurofibroma.
Article in Journal of neuroscience research, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
19 citing papers in PubMed, 27 citations in OpenAlex.
- DKK1 Targeting in Corneal Schwann Cells Rescues Axonal Regeneration and Mechanosensory Function After Corneal Injury.Journal of neuroscience research · 2026Article
- The Role of Sensory Innervation in Homeostatic and Injury-Induced Corneal Epithelial Renewal.International journal of molecular sciences · 2023Review
- Mesenchymal Stem Cell Exosomes as Immunomodulatory Therapy for Corneal Scarring.International journal of molecular sciences · 2023Article
- Schwann Cells Are Key Regulators of Corneal Epithelial Renewal.Investigative ophthalmology & visual science · 2023Article
- Topical Losartan: Practical Guidance for Clinical Trials in the Prevention and Treatment of Corneal Scarring Fibrosis and Other Eye Diseases and Disorders.Journal of ocular pharmacology and therapeutics : the official journal of the Association for Ocular Pharmacology and Therapeutics · 2023Review
- Flavonoids as Strong Inhibitors of MAPK3: A Computational Drug Discovery Approach.International journal of analytical chemistry · 2023Article
- The Yin and Yang of Mesenchymal Cells in the Corneal Stromal Fibrosis Response to Injury: The Cornea as a Model of Fibrosis in Other Organs.Biomolecules · 2022Review
- Combined Therapy Using Human Corneal Stromal Stem Cells and Quiescent Keratocytes to Prevent Corneal Scarring after Injury.International journal of molecular sciences · 2022Article
- Corneal nonmyelinating Schwann cells illuminated by single-cell transcriptomics and visualized by protein biomarkers.Journal of neuroscience research · 2021Article
- Fibroblastic and bone marrow-derived cellularity in the corneal stroma.Experimental eye research · 2021Article
- Corneal myofibroblasts and fibrosis.Experimental eye research · 2020Review
- Quantitative proteomic comparison of myofibroblasts derived from bone marrow and cornea.Scientific reports · 2020Article
- Fibrocytes, Wound Healing, and Corneal Fibrosis.Investigative ophthalmology & visual science · 2020Review
- Coordinated Modulation of Corneal Scarring by the Epithelial Basement Membrane and Descemet's Basement Membrane.Journal of refractive surgery (Thorofare, N.J. : 1995) · 2019Review
- Neuregulin 1 type III improves peripheral nerve myelination in a mouse model of congenital hypomyelinating neuropathy.Human molecular genetics · 2019Article
- Descemet's Membrane Modulation of Posterior Corneal Fibrosis.Investigative ophthalmology & visual science · 2019Article
- Eye of the beholder: Rare eye diseases in focus.Journal of neuroscience research · 2019Review
- The Physicochemical Properties of Decellularized Extracellular Matrix-Coated 3D Printed Poly(ε-caprolactone) Nerve Conduits for Promoting Schwann Cells Proliferation and Differentiation.Materials (Basel, Switzerland) · 2018Article
- Injury and defective regeneration of the epithelial basement membrane in corneal fibrosis: A paradigm for fibrosis in other organs?Matrix biology : journal of the International Society for Matrix Biology · 2017Review
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Recent studies have shown that constitutive activation of extracellular signal-regulated kinases 1 and 2 (ERK1/2) in Schwann cells (SCs) increases myelin thickness in transgenic mice. In this secondary analysis, we report that these transgenic mice develop a postnatal corneal neurofibroma with the loss of corneal transparency by age six months. We show that expansion of non-myelinating SCs, under the control of activated ERK1/2, also drive myofibroblast differentiation that derives from both SC precursors and resident corneal keratocytes. Further, these mice also harbor activated mast cells in the central cornea, which contributes to pathological corneal neovascularization and fibrosis. This breach of corneal avascularity and immune status is associated with the growth of the tumor pannus, resulting in a corneal stroma that is nearly four times its normal size. In corneas with advanced disease, some axons became ectopically myelinated, and the disruption of Remak bundles is evident. To determine whether myofibroblast differentiation was linked to vimentin, we examined the levels and phosphorylation status of this fibrotic biomarker. Concomitant with the early upregulation of vimentin, a serine 38-phosphorylated isoform of vimentin (pSer38vim) increased in SCs, which was attributed primarily to the soluble fraction of protein-not the cytoskeletal portion. However, the overexpressed pSer38vim became predominantly cytoskeletal with the growth of the corneal tumor. Our findings demonstrate an unrecognized function of ERK1/2 in the maintenance of corneal homeostasis, wherein its over-activation in SCs promotes corneal neurofibromas. This study is also the first report of a genetically engineered mouse that spontaneously develops a corneal tumor.
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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.