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Purpose <p>To 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).</p> Study design <p>Experimental.</p> Methods <p>Primary 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 <i>in vitro</i>. HTFs were pre-transfected with ANRIL-specific pcDNA3.1 overexpression vector (ANRIL-OE) for 48&#xa0;h and then treated with TGF-β1 (10&#xa0;ng/mL) for 48&#xa0;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.</p> Results <p>Our 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.</p> Conclusion <p>Collectively, 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.</p>

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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

  • 期刊论文

  • 发表日期：

    2026年7月22日

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

摘要

Purpose

To 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 design

Experimental.

Methods

Primary 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.

Results

Our 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.

Conclusion

Collectively, 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.