International ophthalmology · 2026
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.
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Jiang Lei, Wu Yifeng, Shu Yujie, Fan Fangli, Deng Zhen
Аннотация
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.
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.