由毒蕈碱受体介导的胆碱能信号在培养的黑色素瘤细胞中触发紫外线诱导的黑色素体释放。

IF 3.9 3区 医学 Q2 CELL BIOLOGY Pigment Cell & Melanoma Research Pub Date : 2024-09-30 DOI:10.1111/pcmr.13201
Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim
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引用次数: 0

摘要

在皮肤中,黑色素是在黑色素体中合成和储存的。在表皮黑色素细胞中,黑色素体被运输到邻近的角质形成细胞并被其内化,随后导致皮肤色素沉着。紫外线(UV)辐射会诱导角质形成细胞释放乙酰胆碱(ACh),进而激活邻近黑色素细胞上的乙酰胆碱受体(AChRs),形成 "皮肤突触"。在这里,我们说明了紫外线诱导的 B16F10 黑色素瘤细胞黑色素小体释放可能是由 ACh 共同作用介导的。在细胞培养物中,紫外线照射可强烈诱导黑色素体释放。应用一种毒蕈碱 AChR(mAChR)激动剂--贝特胆(Behanechol,BeCh)可显著增强释放。与此同时,细胞内 Ca2+ 的调动也受到了调节。使用 M1 和/或 M3 mAChRs 拮抗剂可阻断紫外线诱导的黑色素小体释放和细胞内 Ca2+ 的调动。mAChR拮抗剂可抑制紫外线和BeCh处理引发的PKC磷酸化。在紫外线暴露和 mAChR 激动剂的作用下,用于外吞的系留复合物(如 Sec8、Exo70 和 Rab11b)以及突触标记蛋白的表达量增加:M1 或 M3 拮抗剂可完全消除这些诱导作用。在此,我们假设胆碱能信号在紫外线诱导的黑色素体外渗中发挥作用。
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Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells.

In skin, melanin is synthesized and stored in melanosomes. In epidermal melanocytes, melanosomes are transported to and internalized by the neighboring keratinocytes, subsequently leading to skin pigmentation. Ultraviolet (UV) radiation induces the release of acetylcholine (ACh) from keratinocytes, which in turn activates ACh receptors (AChRs) on nearby melanocytes, forming a proposed "skin synapse". Here, we illustrated that the UV-induced melanosome release from cultured B16F10 melanoma cells could be mediated by co-actions of ACh. In the cell cultures, UV exposure robustly elicited melanosome release. Applied bethanechol (BeCh), an agonist of muscarinic AChR (mAChR), could significantly enhance the release. In parallel, the intracellular Ca2+ mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca2+. The phosphorylation of PKC, triggered by UV and BeCh treatments, could be suppressed by the applied mAChR antagonists. The expressions of tethering complex for exocytosis, for example, Sec8, Exo70, and Rab11b, as well as synaptotagmin, were increased under UV exposure together with mAChR agonist: The inductions were fully abolished by M1 or M3 antagonist. Here, we hypothesize that the cholinergic signaling is playing roles in UV-induced exocytosis of melanosomes.

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来源期刊
Pigment Cell & Melanoma Research
Pigment Cell & Melanoma Research 医学-皮肤病学
CiteScore
8.90
自引率
2.30%
发文量
54
审稿时长
6-12 weeks
期刊介绍: Pigment Cell & Melanoma Researchpublishes manuscripts on all aspects of pigment cells including development, cell and molecular biology, genetics, diseases of pigment cells including melanoma. Papers that provide insights into the causes and progression of melanoma including the process of metastasis and invasion, proliferation, senescence, apoptosis or gene regulation are especially welcome, as are papers that use the melanocyte system to answer questions of general biological relevance. Papers that are purely descriptive or make only minor advances to our knowledge of pigment cells or melanoma in particular are not suitable for this journal. Keywords Pigment Cell & Melanoma Research, cell biology, melatonin, biochemistry, chemistry, comparative biology, dermatology, developmental biology, genetics, hormones, intracellular signalling, melanoma, molecular biology, ocular and extracutaneous melanin, pharmacology, photobiology, physics, pigmentary disorders
期刊最新文献
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