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The impact of non-toxic blue light (453 nm) on cellular antioxidative capacity, TGF-β1 signaling, and myofibrogenesis of human skin fibroblasts

细胞内 过氧化氢酶 SMAD公司 活性氧 转化生长因子 MAPK/ERK通路 化学 氧化应激 p38丝裂原活化蛋白激酶 细胞生物学 下调和上调 信号转导 磷酸化 肌成纤维细胞 生物物理学 生物 生物化学 纤维化 医学 内科学 基因
作者
Julia M. Krassovka,Christoph V. Suschek,Max Prost,Vera Grotheer,Jennifer Lynn Schiefer,Erhan Demir,Paul Christian Fuchs,Joachim Windolf,Ewa K. Stürmer,Christian Opländer
出处
期刊:Journal of Photochemistry and Photobiology B-biology [Elsevier BV]
卷期号:209: 111952-111952 被引量:16
标识
DOI:10.1016/j.jphotobiol.2020.111952
摘要

Studies have demonstrated that blue light induces biological effects, such as cell death, and inhibition of proliferation and differentiation. Since blue light at longer wavelength (>440 nm) exerts less injurious effects on cells than at shorter wavelengths, (400–440 nm), we have investigated the impact of non-toxic (LED) blue light at 453 nm wavelength on human skin fibroblasts (hsFBs). We found that besides its decreasing effects on the proliferation rate, repeated blue light irradiations (80 J/cm2) also significantly reduced TGF-β1-induced myofibrogenesis as shown by diminished α-SMA and EDA-FN expression accompanied by reduced protein expression and phosphorylation of ERK 1/2, SMAD 2/3, and p38—key players of TGF-β1-induced myofibrogenesis. In parallel, catalase protein expression, intracellular FAD concentrations as well as NADP+/NADPH ratio were reduced, whereas intracellular reactive oxygen species (ROS) were increased. We postulate that as a molecular mechanism downregulation of catalase and photoreduction of FAD induce intracellular oxidative stress which, in turn, affects the signaling factors of myofibrogenesis leading to a lower rate of α-SMA and EDA-FN expression and, therefore, myofibroblast formation. In conclusion, blue light even at longer wavelengths shows antifibrotic activity and may represent a suitable and safe approach in the treatment of fibrotic skin diseases including hypertrophic scarring and scleroderma.
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