Choi Seoyoung, Yu Eunbi, Park See-Hyoung, Oh Sae Woong, Kwon Kitae, Kim Gyeonghyeon, Ha Heejun, Shin Hee Seon, Min Seokhyeon, Song Minkyung, Cho Jae Youl, Lee Jongsung
Molecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon City, Korea.
Department of Bio and Chemical Engineering, Hongik University, Sejong City, Korea.
Biofactors. 2025 Mar-Apr;51(2):e70015. doi: 10.1002/biof.70015.
Although blue light has been known to negatively affect skin cells, its detailed signaling mechanisms and anti-blue light agents have not been clearly elucidated. We investigated the involvement of Yes-associated protein (YAP)-mediated Hippo signaling in blue light-induced apoptosis, depending on the degree of blue light exposure. Additionally, we elucidated the effects of melatonin on blue light-irradiated keratinocytes and examined their action mechanisms. After blue light irradiation, its effects and antagonizing effects of melatonin on cell proliferation, apoptosis, DNA damage, and transient receptor potential vanilloid 1 (TRPV1)/YAP-mediated signaling were examined in HaCaT cells using western blots, image analysis, flow cytometric analysis, co-immunoprecipitation, and immunocytochemistry. We found that melatonin treatment attenuated the reduced cell viability and increased production of reactive oxygen species (ROS) in response to blue light irradiation. In the experiments to investigate the mechanism of action of blue light and melatonin, we found that YAP changed its binding protein, either p73 or TEAD, depending on the degree of blue light exposure. Melatonin treatment reduced blue light-induced phosphorylation of TRPV1 and MST1/2. Upon treatment with capsazepine, an antagonist of TRPV1, MST1/2 activation also reduced. Furthermore, we found that prolonged blue light irradiation induced DNA damage, which in turn induced YAP-p73 nuclear translocation. These effects were also notably attenuated by melatonin. These findings indicate that depending on the duration of blue light irradiation, two different YAP-mediated Hippo signaling pathways are activated. Additionally, these findings suggest that melatonin could be a potential therapeutic agent for blue light-induced skin damage.
尽管已知蓝光会对皮肤细胞产生负面影响,但其详细的信号传导机制和抗蓝光剂尚未明确阐明。我们研究了Yes相关蛋白(YAP)介导的Hippo信号通路在蓝光诱导的细胞凋亡中的作用,具体取决于蓝光暴露的程度。此外,我们阐明了褪黑素对蓝光照射的角质形成细胞的影响,并研究了其作用机制。蓝光照射后,使用蛋白质免疫印迹、图像分析、流式细胞术分析、免疫共沉淀和免疫细胞化学等方法,检测了褪黑素对HaCaT细胞的细胞增殖、凋亡、DNA损伤以及瞬时受体电位香草酸受体1(TRPV1)/YAP介导的信号通路的影响及其拮抗作用。我们发现,褪黑素处理可减轻蓝光照射引起的细胞活力降低以及活性氧(ROS)生成增加。在研究蓝光和褪黑素作用机制的实验中,我们发现YAP会根据蓝光暴露程度改变其结合蛋白,即p73或TEAD。褪黑素处理可降低蓝光诱导的TRPV1和MST1/2磷酸化。用TRPV1拮抗剂辣椒素处理后,MST1/2的激活也会降低。此外,我们发现长时间蓝光照射会诱导DNA损伤,进而诱导YAP-p73核转位。这些作用也因褪黑素而明显减弱。这些发现表明,根据蓝光照射的持续时间,会激活两种不同的YAP介导的Hippo信号通路。此外,这些发现表明褪黑素可能是治疗蓝光诱导的皮肤损伤的潜在药物。