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首页> 美国卫生研究院文献>other >UVB Stimulates the Expression of Endothelin B Receptor in Human Melanocytes via a Sequential Activation of the p38/MSK1/CREB/MITF Pathway Which Can Be Interrupted by a French Maritime Pine Bark Extract through a Direct Inactivation of MSK1
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UVB Stimulates the Expression of Endothelin B Receptor in Human Melanocytes via a Sequential Activation of the p38/MSK1/CREB/MITF Pathway Which Can Be Interrupted by a French Maritime Pine Bark Extract through a Direct Inactivation of MSK1

机译：UVB通过顺序激活p38 / MSK1 / CREB ​​/ MITF途径刺激人黑素细胞中内皮素B受体的表达该途径可被法国海上松树皮提取物通过直接灭活MSK1中断。

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Melanogenesis is the physiological process by which melanin is synthesized to protect the skin from UV damage. While paracrine interactions between keratinocytes and melanocytes are crucial for regulating epidermal pigmentation, the endothelin (EDN)-endothelin B-receptor (EDNRB) interaction is one of the key linkages. In this study, we found that a single exposure of normal human melanocytes (NHMs) with UVB stimulates the expression of EDNRB and its upstream transcription factor microphthalmia-associated transcription factor (MITF) at the transcriptional and translational levels. That stimulation can be abrogated by post-irradiation treatment with a French maritime pine bark extract (PBE). UVB stimulated the phosphorylation of p38 and c-jun N-terminal kinase (JNK), but not ERK, followed by the increased phosphorylation of MSK1 and CREB. The post-irradiation treatment with PBE did not affect the increased phosphorylation of p38 and JNK, but distinctly abrogated the phosphorylation of MSK1 and CREB. Post-irradiation treatment with the MSK1 inhibitor H89 significantly down-regulated the increased gene expression of MITF and EDNRB in UVB-exposed NHMs. Our findings indicate for the first time that the increased expression of MITF that leads to the up-regulation of melanocyte-specific proteins in UVB-exposed NHMs is mediated via activation of the p38/MSK1/CREB pathway but not the ERK/RSK/CREB pathway. The mode of action by PBE demonstrates that interrupting MSK1 activation is a new target for antioxidants including PBE which can serve as anti-pigmenting agents in a reactive oxygen species-depletion-independent manner.
机译：黑色素生成是合成黑色素以保护皮肤免受紫外线伤害的生理过程。尽管角质形成细胞和黑素细胞之间的旁分泌相互作用对于调节表皮色素沉着至关重要，但内皮素（EDN）-内皮素B受体（EDNRB）相互作用是关键的联系之一。在这项研究中，我们发现正常人黑素细胞（NHMs）与UVB的单次接触会在转录和翻译水平上刺激EDNRB及其上游转录因子小眼症相关转录因子（MITF）的表达。可以通过用法国海上松树皮提取物（PBE）进行辐照后处理来消除这种刺激。 UVB刺激p38和c-jun N末端激酶（JNK）的磷酸化，但不刺激ERK，随后刺激MSK1和CREB的磷酸化增加。用PBE辐照后的处理不会影响p38和JNK的磷酸化增加，但明显废除了MSK1和CREB的磷酸化。用MSK1抑制剂H89进行辐射后处理，显着下调了暴露于UVB的NHMs中MITF和EDNRB的基因表达。我们的发现首次表明，暴露于UVB的NHMs中导致黑素细胞特异性蛋白上调的MITF表达增加是通过激活p38 / MSK1 / CREB途径而不是通过ERK / RSK / CREB介导的。途径。 PBE的作用方式表明，中断MSK1激活是抗氧化剂（包括PBE）的新目标，该抗氧化剂可以以不依赖活性氧的方式独立用作抗色素剂。

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