ArticleInternational journal of ophthalmology2022
Hyperosmolarity disrupts tight junction
Article in International journal of ophthalmology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 23 citations in OpenAlex.
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- Pathological mechanisms of Sjögren's disease-related dry eye: from multiglandular dysfunction to ocular surface inflammation.International ophthalmology · 2026Review
- Therapeutic Effects of Glycyrrhizic Acid on Dry Eye Disease: Targeting Pyroptosis, Oxidative Stress, and Epithelial Barrier Dysfunction.International journal of molecular sciences · 2026Article
- Immuno-inflammatory axis of menopausal dry eye: from hormonal fluctuations to ocular surface dysregulation.Frontiers in immunology · 2026Review
- Managing dry eye disease - a review of selected traditional Chinese medicine and some of their metabolites focusing on molecular mechanisms and signaling pathways.Frontiers in pharmacology · 2026Review
- Depression induces ocular surface inflammation and dry eye-like changes in mice.International journal of ophthalmology · 2026Article
- Triptolide alleviates hyperosmotic stress-induced human corneal epithelial cell damage by inhibiting NLRP3 inflammasome-mediated pyroptosis via the TLR4/NF-κB pathway.Frontiers in medicine · 2026Article
- Atorvastatin improves spermatogenesis in murine and in vitro human chronic orchitis models through restoring blood-testis barriers.Cell death discovery · 2025Article
- Assessing the Independent and Combined Effects of Hyperosmolarity and Inflammatory Stress on Human Corneal Epithelial Cells.Investigative ophthalmology & visual science · 2025Article
- The microenvironment of ocular surface in keratoconus: a systematic review.Eye and vision (London, England) · 2025Review
- Identification of Matrix Metalloproteinase 3 as a Potential Biomarker for Dry Eye Disease.Translational vision science & technology · 2025Article
- Peptide DFCPPGFNTK Mitigates Dry Eye Pathophysiology by Suppressing Oxidative Stress, Apoptosis, Inflammation, and Autophagy: Evidence from In Vitro and In Vivo Models.Current issues in molecular biology · 2025Article
- Efficacy of 0.05% cyclosporine A on tear inflammatory cytokines and goblet cell function after corneal refractive surgery.Journal of ophthalmic inflammation and infection · 2025Article
- Hydroxypropyl-Methylcellulose and GlicoProOphthalmology and therapy · 2025Article
- N-acylethanolamine acid amidase inhibitor-loaded polymeric micelles in the treatment of dry eye disease.International journal of ophthalmology · 2025Article
- Dry eye disease and psychosomatics-benefits of mind-body therapy for dry eye disease.Frontiers in medicine · 2025Review
- Compatibility of a New Ocular Surface Dye with Disposable and Bi-Weekly Soft Contact Lenses: An Experimental Study.Life (Basel, Switzerland) · 2024Article
- The existence of senescent cells in conjunctival epithelium from elderly individuals.Japanese journal of ophthalmology · 2024Article
- Modeling dry eye with an air-liquid interface in corneal epithelium-on-a-chip.Scientific reports · 2024Article
Corrections and comments
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
aimTo investigate the mechanism of the tight junction (TJ) disruption and the association between tumor necrosis factor (TNF)-α and matrix metalloproteinase (MMPs) under hyperosmotic condition in primary human corneal epithelial cells (HCECs).
methodsThe cultured HCECs were exposed to media which adding sodium chloride (NaCl) for hyperosmolar stress or adding rh-TNF-α (10 ng/mL). NF-κB inhibitor (5 µmol/L) or GM-6001 (potent and broad spectrum MMP inhibitor, 20 µmol/L) was added 1h before that treatment. The integrity of TJ proteins was determined by immunofluorescent (IF) staining. The mRNA levels of TNF-α and MMPs were evaluated by quantitative reverse transcription polymerase chain reaction (RT-qPCR) and the protein expression by enzyme-linked immunosorbent assay (ELISA).
resultsTJ proteins ZO-1 and Occludin were disrupted in primary HCECs exposed to hyperosmotic medium. The mRNA expression and protein production of TNF-α increased significantly in hyperosmotic media at 500 mOsM. TNF-α mediated the expression and production of MMP-1, MMP-13, MMP-9, and MMP-3 stimulated by hyperosmotic stress. The production of MMPs in hyperosmolar media were increased through the increase of TNF-α. GM-6001 prevent the destruction of ZO-1 and Occludin in hyperosmolar stress and rh-TNF-α treated medium. TNF-α induced activation of MMPs was involved in the TJ disruption by hyperosmolarity.
conclusionTJ proteins ZO-1 and Occludin are disrupted by hyperosmolar stress and TNF-α, but protected by MMP inhibitor (GM-6001). It suggests that TNF-α/MMP pathway mediates the TJ disruption in primary HCECs exposed to hyperosmotic stress.
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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.