Evidence map›Paper›PMID 42484723›Full record

ArticleInternational ophthalmology2026

LncRNA ANRIL inhibits TGF-β1-induced proliferation, migration, and fibrosis of Tenon's capsule fibroblasts from glaucoma patients by reducing IL-22-RA1 stability and expression.

Lei Jiang, Yifeng Wu, Yujie Shu, Fangli Fan, Zhen Deng

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Article in International 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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5 · Who and what money

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5 authors.

Lei JiangDepartment of Ophthalmology, The First People's Hospital of Linping District, No.369 Yingbin Road, Nanyuan Street, Hangzhou, 311100, Zhejiang, China.
Yifeng WuDepartment of Ophthalmology, The First People's Hospital of Linping District, No.369 Yingbin Road, Nanyuan Street, Hangzhou, 311100, Zhejiang, China.
Yujie ShuDepartment of Ophthalmology, The First People's Hospital of Linping District, No.369 Yingbin Road, Nanyuan Street, Hangzhou, 311100, Zhejiang, China.
Fangli FanDepartment of Ophthalmology, The First People's Hospital of Linping District, No.369 Yingbin Road, Nanyuan Street, Hangzhou, 311100, Zhejiang, China.
Zhen DengDepartment of Ophthalmology, The First People's Hospital of Linping District, No.369 Yingbin Road, Nanyuan Street, Hangzhou, 311100, Zhejiang, China. dengzhenn778@outlook.com.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

purposeTo assess the involvement of long non-coding RNA (lncRNA) Antisense Noncoding RNA in the INK4 Locus (ANRIL) in subconjunctival fibrosis after glaucoma filtration surgery (GFS). STUDY

designExperimental.

methodsPrimary human Tenon's capsule fibroblasts (HTFs) were isolated from glaucoma patients during GFS and then treated with human recombinant protein transforming growth factor-β1 (TGF-β1) to mimic the glaucoma condition in vitro. HTFs were pre-transfected with ANRIL-specific pcDNA3.1 overexpression vector (ANRIL-OE) for 48 h and then treated with TGF-β1 (10 ng/mL) for 48 h, followed by the detection of cell viability, proliferation, and migration by CCK-8 assay, EdU staining, and wound healing assay. The expression of fibrosis markers alpha-smooth muscle actin (α-SMA), fibronectin, and collagen I was determined by RT-qPCR and western blotting. The interaction between ANRIL and interleukin-22 receptor alpha 1 (IL-22-RA1) was verified through RNA pull-down, RNA Immunoprecipitation (RIP), and ubiquitination assays.

resultsOur data revealed that TGF-β1 downregulated ANRIL expression in HTFs. ANRIL overexpression suppressed TGF-β1-induced enhancement in cell viability, proliferation, migration, and extracellular matrix (ECM) deposition in HTFs. Mechanically, ANRIL negatively regulated the stability and expression of IL-22-RA1 by increasing IL-22-RA1 ubiquitination. IL-22-RA1 overexpression antagonized the repressive effects of ANRIL on the proliferation, migration, and fibrosis of TGF-β1-stimulated HTFs.

conclusionCollectively, ANRIL curbs TGF-β1-induced HTF activation and fibrosis by downregulating IL-22-RA1, which provides the rationale for developing strategies based on the ANRIL/IL-22-RA1 axis to prevent scar formation following GFS.

Indexed as

FibroblastsGene Expression RegulationGlaucomaInterleukinsRNA, Long NoncodingTenon CapsuleTransforming Growth Factor beta1Blotting, WesternCell MovementCell ProliferationCells, CulturedFibrosisHumansCDKN2B antisense RNA, humanInterleukinsRNA, Long NoncodingTransforming Growth Factor beta1ANRILGlaucomaIL-22-RA1Tenon’s capsule fibroblastTGF-β1

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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 Socratic graph.