Investigative ophthalmology & visual science · 2025
Therapeutic Potential of Graphene Quantum Dots on Pterygium Cells.
СтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод в очереди
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Koo Donghoon, Kim Minji, Yang Hyun Seung, Kim Jeongmin
Аннотация
PURPOSE: To evaluate the therapeutic potential of graphene quantum dots (GQDs) in modulating key pathological processes in pterygium, including abnormal cell proliferation, migration, and extracellular matrix remodeling.
METHODS: Primary fibroblast cells from human pterygium and conjunctival tissues were cultured and treated with GQDs (6.25-100 µg/mL). Cell cytotoxicity and viability were assessed using live/dead and CCK-8 assays. Cell migration was evaluated via scratch wound-healing assays. Microtubule integrity was analyzed using α-tubulin immunocytochemistry and super-resolution stochastic optical reconstruction microscopy imaging. Expression of pathological proteins (cyclin D1, CDK2, periostin, matrix metalloproteinase [MMP]-3, and MMP-9) was quantified by Western blotting.
RESULTS: GQDs selectively impaired pathological behaviors in pterygium fibroblasts, reducing viability and migration in a dose-dependent manner, with minimal effects on conjunctival fibroblasts. Stochastic optical reconstruction microscopy imaging revealed GQD-induced microtubule fragmentation in pterygium fibroblasts. GQDs also significantly downregulated cyclin D1, CDK2, periostin, MMP-3, and MMP-9.
CONCLUSIONS: GQDs suppress multiple pathologic features of pterygium, including selective cytotoxicity, downregulation of key molecular mediators (cyclin D1, periostin, MMP-3, and MMP-9), and a novel mechanism involving microtubule fragmentation. These findings support the potential of GQDs as a noninvasive therapeutic strategy to suppress pterygium progression and decrease postoperative recurrence.
METHODS: Primary fibroblast cells from human pterygium and conjunctival tissues were cultured and treated with GQDs (6.25-100 µg/mL). Cell cytotoxicity and viability were assessed using live/dead and CCK-8 assays. Cell migration was evaluated via scratch wound-healing assays. Microtubule integrity was analyzed using α-tubulin immunocytochemistry and super-resolution stochastic optical reconstruction microscopy imaging. Expression of pathological proteins (cyclin D1, CDK2, periostin, matrix metalloproteinase [MMP]-3, and MMP-9) was quantified by Western blotting.
RESULTS: GQDs selectively impaired pathological behaviors in pterygium fibroblasts, reducing viability and migration in a dose-dependent manner, with minimal effects on conjunctival fibroblasts. Stochastic optical reconstruction microscopy imaging revealed GQD-induced microtubule fragmentation in pterygium fibroblasts. GQDs also significantly downregulated cyclin D1, CDK2, periostin, MMP-3, and MMP-9.
CONCLUSIONS: GQDs suppress multiple pathologic features of pterygium, including selective cytotoxicity, downregulation of key molecular mediators (cyclin D1, periostin, MMP-3, and MMP-9), and a novel mechanism involving microtubule fragmentation. These findings support the potential of GQDs as a noninvasive therapeutic strategy to suppress pterygium progression and decrease postoperative recurrence.