ArticleJournal of inflammation research2022
Long Noncoding RNA MIAT Regulates Hyperosmotic Stress-Induced Corneal Epithelial Cell Injury via Inhibiting the Caspase-1-Dependent Pyroptosis and Apoptosis in Dry Eye Disease.
Article in Journal of inflammation research, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 24 citations in OpenAlex.
- Inhibition of SGK1 Alleviates Apoptosis and Oxidative Stress in Dry Eye Disease by Activating FoxO3a-Mediated Autophagy.Investigative ophthalmology & visual science · 2026Article
- 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
- Bisphenol A exacerbates dry eye disease via the CASP1/GSDMD-mediated pyroptotic axis: network toxicology, mendelian randomization, and experimental validation.Frontiers in pharmacology · 2026Article
- Upregulations of SNAT2 and GLS-1 Are Key Osmoregulatory Responses of Human Corneal Epithelial Cells to Hyperosmotic Stress.Journal of proteome research · 2025Article
- Role of Chinese Medicine Monomers in Dry Eye Disease: Breaking the Vicious Cycle of Inflammation.Pharmacology research & perspectives · 2025Review
- Neutrophil pyroptosis regulates corneal wound healing and post-injury neovascularisation.Clinical and translational medicine · 2024Article
- LncRNA MIAT suppresses inflammation in LPS-induced J774A.1 macrophages by promoting autophagy through miR-30a-5p/SOCS1 axi.Scientific reports · 2024Article
- IL-1β induced down-regulation of miR-146a-5p promoted pyroptosis and apoptosis of corneal epithelial cell in dry eye disease through targeting STAT3.BMC ophthalmology · 2024Article
- Dopamine Receptor 1 Treatment Promotes Epithelial Repair of Corneal Injury by Inhibiting NOD-Like Receptor Protein 3-Associated Inflammation.Investigative ophthalmology & visual science · 2024Article
- Astaxanthin activated the SLC7A11/GPX4 pathway to inhibit ferroptosis and enhance autophagy, ameliorating dry eye disease.Frontiers in pharmacology · 2024Article
- The alterations of ocular surface metabolism and the related immunity inflammation in dry eye.Advances in ophthalmology practice and researchReview
Corrections and comments
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Authors and funding
7 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Purpose: The biological role and mechanism of long noncoding RNA (lncRNA) myocardial infarction-associated transcript (MIAT) in dry eye remain to be illustrated. Pyroptosis is a noticeable form of inflammatory activation, which is characteristic of gasdermin D (GSDMD)-driven cell death. The present study was designed to explore the role of MIAT in pyroptosis and apoptosis induced by hyperosmolarity stress (HS) in human corneal epithelial cells (HCECs). Methods: HCECs were cultured in 70-120 mM hyperosmotic medium for 24 h to create a dry eye model in vitro. The level of the pyroptosis marker GSDMD was measured, and the cell inflammatory response was evaluated by detecting IL-1β and IL-18 levels. Exogenous caspase-1 inhibitor Ac-YVAD-CHO was used. The pyroptosis in HCECs was examined by caspase-1 activity, immunofluorescent staining, and Western blotting. Flow cytometry was performed to test the apoptosis rate of HCECs. Cell migration and proliferation were detected. The expression of the lncRNA MIAT in HCECs was detected by quantitative real-time PCR. MIAT was knocked down by small interfering RNA (siRNA) transfection. The effects of caspase-1 inhibition on pyroptosis, apoptosis, migration, and proliferation were observed. Results: HS promoted pyroptosis in HCECs by elevating caspase-1, GSDMD, and the active cleavage of GSDMD (N-terminal domain, N-GSDMD), and increased the release of IL-1β, IL-18, LDH and the rate of apoptosis, with reduced cell migration. These changes were prevented by the inhibition of caspase-1. The expression of MIAT was significantly increased in HCECs exposed to a hyperosmotic medium. Silencing MIAT increased the expression of GSDMD, caspase-1, and inflammatory chemokines IL-1β and IL-18, and promoted apoptosis while inhibiting migration and proliferation in HCECs. Conclusion: The lncRNA MIAT is involved in HS-induced pyroptosis and apoptosis and the inflammatory response of HCECs and provides a new understanding of the pathogenesis of dry eye.
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