ArticleInvestigative ophthalmology & visual science2025
Targeting miR-184 to Enhance Corneal Epithelial Wound Healing: In Vivo Knockout, Antisense Inhibition, and Exosome-Mediated Delivery.
Article in Investigative ophthalmology & visual science, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
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Who cites it
4 citing papers in PubMed.
- Altered expression of miRNAs and its implication for Pseudomonas aeruginosa keratitis.Indian journal of ophthalmology · 2026Article
- mRNA and microRNA Expression Profile of Corneal and Conjunctival Impression Cytology Samples.Biology · 2026Article
- The +57C>T substitution in microRNA-184 is associated with microphthalmia, retinal detachment, and altered ocular development.medRxiv : the preprint server for health sciences · 2026Article
- Research progress on the mechanism, diagnosis, and treatment of exosomal miRNA in chronic prostatitis.Frontiers in immunology · 2026Review
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Authors and funding
5 authors.
Funding
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Abstract
Purpose: MicroRNA-184 (miR-184) is known to negatively regulate corneal epithelial wound healing (CEWH) by modulating target genes. This study aimed to further investigate its role in vivo and explore potential therapeutic strategies targeting miR-184 to promote CEWH. Methods: Corneal epithelial-specific Mir184 conditional knockout (cKO) mice were generated using the Cre/loxP system. CEWH was evaluated by fluorescein slit-lamp imaging and histology. Epithelial cell proliferation and cell cycle progression were assessed by in vivo EdU incorporation and flow cytometry, respectively. Planar and vertical cell migration were examined using in vitro scratch assays and an in vivo EdU pulse-chase assay. Expression levels of miR-184 and its targets were measured by RT-qPCR and Western blot analysis. Therapeutic inhibition of miR-184 was achieved through intrastromal locked nucleic acid (LNA)-anti-miR-184 injection, soluble drug-loaded microneedle patches, or exosome-mediated delivery in CEWH mouse models. Results: Corneal epithelial-specific deletion of miR-184 significantly accelerated CEWH, enhanced epithelial cell proliferation, and promoted cell cycle progression compared with wild-type controls. MiR-184 deletion accelerated corneal epithelial turnover in vivo and enhanced in vitro epithelial cell migration. Loss of miR-184 led to upregulation of target proteins CDC25A, CARM1, and LASP1. Therapeutic inhibition of miR-184 via intrastromal LNA-anti-miR-184, soluble microneedle patches, or exosome-mediated delivery recapitulated the genetic phenotype, promoting CEWH, reducing miR-184 levels, and increasing target protein expression. Conclusions: Genetic deletion or therapeutic inhibition of miR-184 promotes CEWH via derepression of target genes. Microneedles and exosome-based delivery represent promising translational approaches to enhance CEWH.
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