蓝光的色素沉着是通过 OPN3-TRPV1 激活黑色素生成和抑制自噬介导的。

Eunbi Yu, Sae Woong Oh, See-Hyoung Park, Kitae Kwon, Su Bin Han, Su Hyun Kang, Jung Hyun Lee, Heejun Ha, Donghoon Yoon, Eunsun Jung, Minkyung Song, Jae Youl Cho, Jongsung Lee
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引用次数: 0

摘要

蓝光是可见光光谱中的一种高能辐射,最近有报道称它能诱导皮肤色素沉着。在这项研究中,我们研究了TRPV1介导的信号传导与OPN3在蓝光诱导的黑色素生成中的参与及其信号传导途径。OPN3是蓝光诱导黑色素生成的下游靶点,蓝光激活TRPV1并上调其表达,导致钙离子流入。[Ca2+]诱导激活 CaMKII 和 MAPK。它还下调了簇蛋白的表达,导致 PAX3 的核转位,最终影响黑色素的合成。此外,蓝光不仅降低了CLU和LC3B之间的相互作用,还降低了ATF家族的表达,从而干扰了自噬介导的黑色素体调节。这些研究结果表明,蓝光的色素沉着作用是由CaMKII和MAPK介导的信号传导以及CLU通过OPN3-TRPV1-钙离子流入对自噬的依赖性抑制所介导的,这表明蓝光调节黑色素细胞生物学的一个新的信号传导途径。此外,这些结果表明,TRPV1和CLU可能是蓝光诱导的色素沉着的潜在治疗靶点。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
The Pigmentation of Blue Light Is Mediated by Both Melanogenesis Activation and Autophagy Inhibition through OPN3-TRPV1.

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.

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