Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2025
TRIM69 alleviates ultraviolet B irradiation-induced ferroptosis by regulating p53 in human lens epithelial cells.
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Sun Yang, Ainiwaer Maierdanjiang, Xiao Binghe, Hong Yingying, Ning Li, Ji Yinghong
Аннотация
PURPOSE: Age-related cataract (ARC) is the leading cause of visual impairment worldwide, with ultraviolet B (UVB) radiation recognized as a major risk factor. This study aimed to investigate whether UVB induces ferroptosis in human lens epithelial cells (HLECs) and to explore the role of TRIM69 in modulating this process through the p53 signaling pathway.
METHODS: HLECs were exposed to UVB irradiation, and ferroptosis was assessed by measuring cell viability, reactive oxygen species (ROS) accumulation, glutathione peroxidase 4 (GPX4) expression, and glutathione (GSH) levels. Ferroptosis inhibition was examined using ferrostatin-1 (Fer-1). TRIM69 expression was modulated by overexpression and knockdown, while the interaction with p53 signaling was evaluated through p53 overexpression assays. Western blotting was performed to analyze GPX4 and SLC7A11 expression.
RESULTS: UVB exposure induced ferroptosis in HLECs, evidenced by reduced GPX4 and GSH, elevated ROS, and decreased viability. Fer-1 treatment significantly improved cell viability and suppressed ROS accumulation. TRIM69 overexpression significantly mitigated the effects of UVB irradiation on cell viability, GSH levels and ROS production, whereas knocking down TRIM69 expression exacerbated these effects. Importantly, p53 overexpression reversed the protective effects of TRIM69 and downregulated GPX4 and SLC7A11, implicating p53-dependent signaling in ferroptosis regulation.
CONCLUSION: These findings demonstrate that TRIM69 protects HLECs against UVB-induced ferroptosis by inhibiting p53-mediated suppression of GPX4 and SLC7A11. TRIM69 may represent a promising therapeutic target for preventing oxidative damage and delaying the onset of ARC.
METHODS: HLECs were exposed to UVB irradiation, and ferroptosis was assessed by measuring cell viability, reactive oxygen species (ROS) accumulation, glutathione peroxidase 4 (GPX4) expression, and glutathione (GSH) levels. Ferroptosis inhibition was examined using ferrostatin-1 (Fer-1). TRIM69 expression was modulated by overexpression and knockdown, while the interaction with p53 signaling was evaluated through p53 overexpression assays. Western blotting was performed to analyze GPX4 and SLC7A11 expression.
RESULTS: UVB exposure induced ferroptosis in HLECs, evidenced by reduced GPX4 and GSH, elevated ROS, and decreased viability. Fer-1 treatment significantly improved cell viability and suppressed ROS accumulation. TRIM69 overexpression significantly mitigated the effects of UVB irradiation on cell viability, GSH levels and ROS production, whereas knocking down TRIM69 expression exacerbated these effects. Importantly, p53 overexpression reversed the protective effects of TRIM69 and downregulated GPX4 and SLC7A11, implicating p53-dependent signaling in ferroptosis regulation.
CONCLUSION: These findings demonstrate that TRIM69 protects HLECs against UVB-induced ferroptosis by inhibiting p53-mediated suppression of GPX4 and SLC7A11. TRIM69 may represent a promising therapeutic target for preventing oxidative damage and delaying the onset of ARC.