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蓝光色素沉着是通过OPN3-TRPV1介导的黑素生成激活和自噬抑制实现的。

The Pigmentation of Blue Light Is Mediated by Both Melanogenesis Activation and Autophagy Inhibition through OPN3-TRPV1.

作者信息

Yu Eunbi, Oh Sae Woong, Park See-Hyoung, Kwon Kitae, Han Su Bin, Kang Su Hyun, Lee Jung Hyun, Ha Heejun, Yoon Donghoon, Jung Eunsun, Song Minkyung, Cho Jae Youl, Lee Jongsung

机构信息

Molecular Dermatology Laboratory, Department of Integrative Biotechnology, College of Biotechnology and Bioengineering, Sungkyunkwan University, Suwon, Korea.

Department of Bio and Chemical Engineering, Hongik University, Sejong City, Korea.

出版信息

J Invest Dermatol. 2025 Apr;145(4):908-918.e6. doi: 10.1016/j.jid.2024.07.034. Epub 2024 Sep 4.

DOI:10.1016/j.jid.2024.07.034
PMID:39241981
Abstract

Blue light, a high-energy radiation in the visible light spectrum, was recently reported to induce skin pigmentation. In this study, we investigated the involvement of TRPV1-mediated signaling along with OPN3 in blue light-induced melanogenesis as well as its signaling pathway. Operating downstream target of OPN3 in blue light-induced melanogenesis, blue light activated TRPV1 and upregulated its expression, resulting in calcium influx. Calcium ion induced the activation of calcium/calmodulin-dependent protein kinase II and MAPK. It also downregulated clusterin expression, leading to the nuclear translocation of PAX3, ultimately affecting melanin synthesis. In addition, blue light interfered with autophagy-mediated regulation of melanosomes by decreasing not only the interaction between clusterin and LC3B but the expression of activating transcription factor family. These findings demonstrate that the pigmenting effects of blue light are mediated by calcium/calmodulin-dependent protein kinase II- and MAPK-mediated signaling as well as clusterin-dependent inhibition of autophagy through OPN3-TRPV1-calcium influx, suggesting, to our knowledge, a previously unreported signaling pathway through which blue light regulates melanocyte biology. Furthermore, these results suggest that TRPV1 and clusterin could be potential therapeutic targets for blue light-induced pigmentation due to prolonged exposure to blue light.

摘要

蓝光是可见光谱中的一种高能辐射,最近有报道称其可诱导皮肤色素沉着。在本研究中,我们研究了TRPV1介导的信号传导以及OPN3在蓝光诱导的黑色素生成中的作用及其信号通路。作为OPN3在蓝光诱导的黑色素生成中的下游作用靶点,蓝光激活TRPV1并上调其表达,导致钙离子内流。钙离子诱导钙/钙调蛋白依赖性蛋白激酶II和丝裂原活化蛋白激酶(MAPK)的激活。它还下调簇集素的表达,导致PAX3的核转位,最终影响黑色素合成。此外,蓝光不仅通过减少簇集素与LC3B之间的相互作用,还通过降低激活转录因子家族的表达来干扰自噬介导的黑素小体调节。这些发现表明,蓝光的色素沉着作用是由钙/钙调蛋白依赖性蛋白激酶II和MAPK介导的信号传导以及通过OPN3-TRPV1-钙离子内流的簇集素依赖性自噬抑制所介导的,据我们所知,这提示了一条以前未报道的蓝光调节黑素细胞生物学的信号通路。此外,这些结果表明,由于长期暴露于蓝光,TRPV1和簇集素可能是蓝光诱导色素沉着的潜在治疗靶点。

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