ArticleThe American journal of pathology2019
Inflammatory Stress Causes N-Glycan Processing Deficiency in Ocular Autoimmune Disease.
Article in The American journal of pathology, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 27 citations in OpenAlex.
- Nanosuspension-based Ocular Therapeutics for Infection Control: Integrating Mucin Interactions and Tear Film Dynamics.AAPS PharmSciTech · 2026Review
- Ocular surface glycocalyx in health and disease.Frontiers in cell and developmental biology · 2025Review
- Tissue Remodeling in Ocular Mucous Membrane Pemphigoid.Investigative ophthalmology & visual science · 2023Observational
- Characterization of aberrant glycosylation associated with osteoarthritis based on integrated glycomics methods.Arthritis research & therapy · 2023Article
- Exon-intron split analysis reveals posttranscriptional regulatory signals induced by high and low n-6/n-3 polyunsaturated fatty acid ratio diets in piglets.Journal of animal science · 2023Article
- Glycogene Expression Profile of Human Limbal Epithelial Cells with Distinct Clonogenic Potential.Cells · 2022Article
- Membrane-associated mucins of the human ocular surface in health and disease.The ocular surface · 2021Review
- Galectins as Regulators of Corneal Inflammation.Current opinion in physiology · 2021Article
- The Epithelial Cell Glycocalyx in Ocular Surface Infection.Frontiers in immunology · 2021Review
- Disrupted Glycocalyx as a Source of Ocular Surface Biomarkers.Eye & contact lens · 2020Review
- Endoplasmic reticulum stress promotes inflammation-mediated proteolytic activity at the ocular surface.Scientific reports · 2020Article
- Distribution and Function of Glycosaminoglycans and Proteoglycans in the Development, Homeostasis and Pathology of the Ocular Surface.Frontiers in cell and developmental biology · 2020Review
- Article
Corrections and comments
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Authors and funding
7 authors at 6 institutions in 3 countries.
Funding
Abstract
High levels of proinflammatory cytokines have been associated with a loss of tissue function in ocular autoimmune diseases, but the basis for this relationship remains poorly understood. Here we investigate a new role for tumor necrosis factor α in promoting N-glycan-processing deficiency at the surface of the eye through inhibition of N-acetylglucosaminyltransferase expression in the Golgi. Using mass spectrometry, complex-type biantennary oligosaccharides were identified as major N-glycan structures in differentiated human corneal epithelial cells. Remarkably, significant differences were detected between the efficacies of cytokines in regulating the expression of glycogenes involved in the biosynthesis of N-glycans. Tumor necrosis factor α but not IL-1β had a profound effect in suppressing the expression of enzymes involved in the Golgi branching pathway, including N-acetylglucosaminyltransferases 1 and 2, which are required for the formation of biantennary structures. This decrease in gene expression was correlated with a reduction in enzymatic activity and impaired N-glycan branching. Moreover, patients with ocular mucous membrane pemphigoid were characterized by marginal N-acetylglucosaminyltransferase expression and decreased N-glycan branching in the conjunctiva. Together, these data indicate that proinflammatory cytokines differentially influence the expression of N-glycan-processing enzymes in the Golgi and set the stage for future studies to explore the pathophysiology of ocular autoimmune diseases.
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Registered trials
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