Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim
{"title":"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。","authors":"Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim","doi":"10.1111/pcmr.13201","DOIUrl":null,"url":null,"abstract":"<p><p>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 Ca<sup>2+</sup> mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca<sup>2+</sup>. 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.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":null,"pages":null},"PeriodicalIF":3.9000,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":"{\"title\":\"Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells.\",\"authors\":\"Maggie Suisui Guo, Qiyun Wu, Yingjie Xia, Jiahui Wu, Xiaoyang Wang, Gary Ka Wing Yuen, Tina Tingxia Dong, Jin Gao, Karl Wah Keung Tsim\",\"doi\":\"10.1111/pcmr.13201\",\"DOIUrl\":null,\"url\":null,\"abstract\":\"<p><p>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 Ca<sup>2+</sup> mobilization was regulated. The applied antagonists of M1 and/or M3 mAChRs could block the UV-induced melanosome release and the mobilization of intracellular Ca<sup>2+</sup>. 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.</p>\",\"PeriodicalId\":219,\"journal\":{\"name\":\"Pigment Cell & Melanoma Research\",\"volume\":null,\"pages\":null},\"PeriodicalIF\":3.9000,\"publicationDate\":\"2024-09-30\",\"publicationTypes\":\"Journal Article\",\"fieldsOfStudy\":null,\"isOpenAccess\":false,\"openAccessPdf\":\"\",\"citationCount\":\"0\",\"resultStr\":null,\"platform\":\"Semanticscholar\",\"paperid\":null,\"PeriodicalName\":\"Pigment Cell & Melanoma Research\",\"FirstCategoryId\":\"3\",\"ListUrlMain\":\"https://doi.org/10.1111/pcmr.13201\",\"RegionNum\":3,\"RegionCategory\":\"医学\",\"ArticlePicture\":[],\"TitleCN\":null,\"AbstractTextCN\":null,\"PMCID\":null,\"EPubDate\":\"\",\"PubModel\":\"\",\"JCR\":\"Q2\",\"JCRName\":\"CELL BIOLOGY\",\"Score\":null,\"Total\":0}","platform":"Semanticscholar","paperid":null,"PeriodicalName":"Pigment Cell & Melanoma Research","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1111/pcmr.13201","RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"CELL BIOLOGY","Score":null,"Total":0}
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.
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