ArticleInvestigative ophthalmology & visual science2022
Corneal Epithelium-Derived Netrin-1 Alleviates Dry Eye Disease via Regulating Dendritic Cell Activation.
Article in Investigative ophthalmology & visual science, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 16 citations in OpenAlex.
- MSC-encapsulated porous microparticle eye drops for autoimmune dry eye disease treatment in NOD mice.Science advances · 2025Article
- Prox1 Protein in Corneal Limbal Lymphatic Vessels Maintains Limbal Stem Cell Stemness and Regulates Corneal Injury Repair.Investigative ophthalmology & visual science · 2025Article
- Advanced Biomaterials for Lacrimal Tissue Engineering: A Review.Materials (Basel, Switzerland) · 2024Review
- A Novel Murine Model for Lupus-Like Ocular Chronic Graft-Versus-Host Disease.Investigative ophthalmology & visual science · 2024Article
- Transmembrane Protein CMTM6 Alleviates Ocular Inflammatory Response and Improves Corneal Epithelial Barrier Function in Experimental Dry Eye.Investigative ophthalmology & visual science · 2024Article
- Ocular surface immune cell diversity in dry eye disease.Indian journal of ophthalmology · 2023Review
- Suppression of NLRP3/Caspase-1/GSDMD Mediated Corneal Epithelium Pyroptosis Using Melatonin-Loaded Liposomes to Inhibit Benzalkonium Chloride-Induced Dry Eye Disease.International journal of nanomedicine · 2023Article
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Authors and funding
8 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: To investigate the expression of corneal epithelium-derived netrin-1 (NTN-1) and its immunoregulatory function in dry eye disease (DED) using a DED mouse model. Methods: We generated DED mouse models with desiccating stress under scopolamine treatment. RNA sequencing was performed to identify differentially expressed genes (DEGs) in the corneal epithelium of DED mice. NTN-1 expression was analyzed via real-time PCR, immunofluorescence staining, and immunoblotting. The DED mice were then treated with recombinant NTN-1 or neutralizing antibodies to investigate the severity of the disease, dendritic cell (DC) activation, and inflammatory cytokine expression. Results: A total of 347 DEGs (292 upregulated and 55 downregulated) were identified in the corneal epithelium of DED mice: corneal epithelium-derived NTN-1 expression was significantly decreased in DED mice compared to that in control mice. Topical recombinant NTN-1 application alleviated the severity of the disease, accompanied by restoration of tear secretion and goblet cell density. In addition, NTN-1 decreased the number of DCs, inhibited the activation of the DCs and Th17 cells, and reduced the expression of inflammatory factors in DED mice. In contrast, blocking endogenous NTN-1 activity with an anti-NTN-1 antibody aggravated the disease, enhanced DC activation, and upregulated the inflammatory factors in the conjunctivae of DED mice. Conclusions: We identified decreased NTN-1 expression in the corneal epithelium of DED mice. Our findings elucidate the role of NTN-1 in alleviating DED and impeding DC activation, thereby indicating its therapeutic potential in suppressing ocular inflammation in DED.
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