Advances in clinical and experimental medicine : official organ Wroclaw Medical University · 2026
Integrin β3 knockdown suppresses TGF-β2-induced migration and epithelial-mesenchymal transition in human lens epithelial cells.
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Lin Chengmin, Chen Lu
Аннотация
BACKGROUND: Posterior capsular opacification (PCO) is a common complication of cataract surgery and is strongly associated with the epithelial-mesenchymal transition (EMT) of lens epithelial cells (LECs). Integrin β3 (ITGB3) has been implicated in various pathological processes; however, its role in PCO remains insufficiently understood.
OBJECTIVES: To investigate the regulatory role of ITGB3 in PCO progression and determine whether ITGB3 modulates transforming growth factor-β2 (TGF-β2)-induced migration and EMT in human lens epithelial cells.
MATERIAL AND METHODS: Human lens epithelial HLE-B3 cells were treated with transforming growth factor-β2 (TGF-β2; 10 ng/mL) to establish an in vitro model of PCO. ITGB3 expression at the mRNA and protein levels was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Cell proliferation was evaluated using the 5-ethynyl-2'-deoxyuridine (EdU) assay, while cell migration was assessed using transwell and wound-healing assays.
RESULTS: TGF-β2 stimulation significantly increased ITGB3 expression in HLE-B3 cells. Silencing of ITGB3 significantly reduced the proliferation of TGF-β2-treated cells and inhibited their migratory capacity, as demonstrated by both transwell and wound-healing assays. Exposure to TGF-β2 promoted EMT, whereas ITGB3 knockdown reversed this effect. Furthermore, activation of the TGF-β/Smad2/3 signaling pathway induced by TGF-β2 was attenuated following ITGB3 silencing.
CONCLUSIONS: Knockdown of ITGB3 alleviates TGF-β2-induced migration and EMT in HLE-B3 cells by suppressing the TGF-β/Smad2/3 signaling pathway, supporting ITGB3 as a potential therapeutic target for the prevention and treatment of PCO.
OBJECTIVES: To investigate the regulatory role of ITGB3 in PCO progression and determine whether ITGB3 modulates transforming growth factor-β2 (TGF-β2)-induced migration and EMT in human lens epithelial cells.
MATERIAL AND METHODS: Human lens epithelial HLE-B3 cells were treated with transforming growth factor-β2 (TGF-β2; 10 ng/mL) to establish an in vitro model of PCO. ITGB3 expression at the mRNA and protein levels was assessed using reverse transcription quantitative polymerase chain reaction (RT-qPCR) and western blotting. Cell proliferation was evaluated using the 5-ethynyl-2'-deoxyuridine (EdU) assay, while cell migration was assessed using transwell and wound-healing assays.
RESULTS: TGF-β2 stimulation significantly increased ITGB3 expression in HLE-B3 cells. Silencing of ITGB3 significantly reduced the proliferation of TGF-β2-treated cells and inhibited their migratory capacity, as demonstrated by both transwell and wound-healing assays. Exposure to TGF-β2 promoted EMT, whereas ITGB3 knockdown reversed this effect. Furthermore, activation of the TGF-β/Smad2/3 signaling pathway induced by TGF-β2 was attenuated following ITGB3 silencing.
CONCLUSIONS: Knockdown of ITGB3 alleviates TGF-β2-induced migration and EMT in HLE-B3 cells by suppressing the TGF-β/Smad2/3 signaling pathway, supporting ITGB3 as a potential therapeutic target for the prevention and treatment of PCO.