ArticleInternational journal of ophthalmology2026
Vaccinia-related kinase 1/snail family transcriptional repressor 1 regulates epithelial-mesenchymal transition and inflammation in proliferative vitreoretinopathy.
Article in International journal of ophthalmology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.
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Abstract
aimTo investigate whether vaccinia-related kinase 1 (VRK1) mediates transforming growth factor-beta2 (TGF-β2)-caused epithelial-mesenchymal transition (EMT) and inflammatory responses in retinal pigment epithelial (RPE) cells through regulating snail family transcriptional repressor 1 (SNAI1), and to validate its role in a proliferative vitreoretinopathy (PVR) mouse model.
methodsHuman RPE cell line ARPE-19 cells were treated with TGF-β2 to construct an EMT model. Western blot detected VRK1 level. The effects of VRK1 on SNAI1 expression and biological behavior of ARPE-19 cells were detected by immunofluorescence, ELISA, Transwell, and scratch assay, and the interaction between VRK1 and SNAI1 was confirmed through immunoprecipitation. A PVR mouse model was constructed, and the effects of VRK1 or/and SNAI1 on retinal damage were assessed by pathologic staining. Inflammatory factors and EMT-related proteins were assessed with ELISA and Western blot.
resultsVRK1 was upregulated in ARPE-19 cells after TGF-β2 treatment. Overexpression of VRK1 increased cell viability, promoted cell migration and EMT, and the levels of inflammatory factors. Silencing of VRK1 reversed the above indexes. There was a direct interaction between VRK1 and SNAI1, and overexpresssion SNAI1 weakened the impacts of silencing of VRK1. In PVR mice, silencing of VRK1 ameliorated retinal structural damage, decreased proinflammatory factor levels, and suppressed SNAI1 and mesenchymal marker expression. SNAI1 overexpression antagonized the protective effects of silencing VRK1 and exacerbated EMT and inflammatory responses.
conclusionVRK1 plays a key role in retinal structural and inflammatory damage in PVR mice by regulating SNAI1 and mediating TGF-β2-caused EMT and inflammatory responses in RPE cells.
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