Targeting miR-184 to Enhance Corneal Epithelial Wound Healing: In Vivo Knockout, Antisense Inhibition, and Exosome-Mediated Delivery
Cao Q., Wang J., Xu W., Reinach PS., Yan D.
Animal Study on Chronic Wound, published in Invest Ophthalmol Vis Sci (2025) — summary generated from the PubMed abstract.
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
- Level A · Stronger Clinical Evidence
- Level B · Emerging clinical evidence with positive signals
- Level C · Early human research exploring benefits
- Level D · Scientific groundwork from lab and animal studies
- Emerging · Emerging topic under active research
This page is generated from the PubMed record. The Thai description is an automated summary of bibliographic fields and the abstract, not a full translation, and is not medical advice.
- Study type
- Animal Study
- Journal
- Invest Ophthalmol Vis Sci (2025)
- Reported sample size
- —
- Source database
- Europe PMC
- PMID
- 41196130
- PMCID
- PMC12599515
- DOI
- 10.1167/iovs.66.14.13
Abstract (original English)
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 LASP
What this study does not prove
- • This study does not prove SVF is an approved treatment or a replacement for standard care.
- • This is preclinical work; animal or laboratory results cannot be applied to humans.
Evidence level
Evidence from laboratory and animal studies provides groundwork for understanding mechanisms and potential before human studies continue.
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