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Aquaporin-8 promotes human dermal fibroblasts to counteract hydrogen peroxide-induced oxidative damage: A novel target for management of skin aging
Open Life Sciences ( IF 2.2 ) Pub Date : 2024-02-16 , DOI: 10.1515/biol-2022-0828
Shu-Hsiang Liu, Wei-Chun Lin, En-Chih Liao, Yung-Feng Lin, Ching-Shuen Wang, Sheng-Yang Lee, Dee Pei, Chun-Hsien Hsu

The skin is subjected to various external factors that contribute to aging including oxidative stress from hydrogen peroxide (H2O2). This study investigated the distribution of aquaporin-8 (AQP8), a protein that transports H2O2 across biological membranes, in skin cells, and its effects in mitigating H2O2-induced oxidative damage. Human dermal fibroblasts were treated with increasing concentrations of H2O2 to evaluate oxidative damage. Cell viability, reactive oxygen species (ROS) generation, and the expression of specific genes associated with skin aging (IL-10, FPR2, COL1A1, KRT19, and Aggrecan) were evaluated and AQP8 expression was assessed via quantitative polymerase chain reaction and western blotting. Small-interfering RNA was used to silence the AQP8 gene and evaluate its significance. The results show that H2O2 treatment reduces cell viability and increases ROS generation, leading to oxidative damage that affects the expression of target molecules. Interestingly, H2O2-treated cells exhibit high levels of AQP8 expression and gene silencing of AQP8 reverses high levels of ROS and low levels of COL1A1, KRT19, and Aggrecan expression in stressed cells, indicating that AQP8 plays a vital role in preventing oxidative damage and consequent aging. In conclusion, AQP8 is upregulated in human dermal fibroblasts during H2O2-induced oxidative stress and may help prevent oxidative damage and aging. These findings suggest that AQP8 could be a potential therapeutic target for skin aging. Further research is necessary to explore the feasibility of using AQP8 as a preventive or therapeutic strategy for maintaining skin health.

中文翻译:

Aquaporin-8 促进人真皮成纤维细胞抵抗过氧化氢引起的氧化损伤:皮肤衰老管理的新靶点

皮肤会受到各种导致衰老的外部因素的影响,包括过氧化氢(H22)。本研究调查了水通道蛋白 8 (AQP8) 的分布,水通道蛋白 8 是一种转运 H 的蛋白质。22跨生物膜、皮肤细胞及其减轻 H 的作用22- 诱导的氧化损伤。用浓度不断增加的 H 处理人真皮成纤维细胞22评估氧化损伤。评估细胞活力、活性氧 (ROS) 生成以及与皮肤衰老相关的特定基因(IL-10、FPR2、COL1A1、KRT19 和 Aggrecan)的表达,并通过定量聚合酶链反应和蛋白质印迹评估 AQP8 表达。使用小干扰RNA沉默AQP8基因并评估其意义。结果表明,H22治疗会降低细胞活力并增加 ROS 的产生,导致氧化损伤,从而影响靶分子的表达。有趣的是,H22处理的细胞表现出高水平的 AQP8 表达,AQP8 的基因沉默可逆转应激细胞中高水平的 ROS 和低水平的 COL1A1、KRT19 和聚集蛋白聚糖表达,表明 AQP8 在防止氧化损伤和随后的衰老中发挥着至关重要的作用。总之,H 期间人真皮成纤维细胞中 AQP8 上调22-诱导氧化应激,可能有助于防止氧化损伤和衰老。这些发现表明 AQP8 可能是皮肤衰老的潜在治疗靶点。需要进一步的研究来探索使用 AQP8 作为维持皮肤健康的预防或治疗策略的可行性。
更新日期:2024-02-16
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