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The Lipid Droplet Protein DHRS3 Is a Regulator of Melanoma Cell State. 脂滴蛋白 DHRS3 是黑色素瘤细胞状态的调控因子
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-31 DOI: 10.1111/pcmr.13208
Eleanor Johns, Yilun Ma, Pakavarin Louphrasitthiphol, Christopher Peralta, Miranda V Hunter, Jeremy H Raymond, Henrik Molina, Colin R Goding, Richard M White

Lipid droplets are fat storage organelles composed of a protein envelope and lipid-rich core. Regulation of this protein envelope underlies differential lipid droplet formation and function. In melanoma, lipid droplet formation has been linked to tumor progression and metastasis, but it is unknown whether lipid droplet proteins play a role. To address this, we performed proteomic analysis of the lipid droplet envelope in melanoma. We found that lipid droplet proteins were differentially enriched in distinct melanoma states; from melanocytic to undifferentiated. DHRS3, which converts all-trans-retinal to all-trans-retinol, is upregulated in the MITFLO/undifferentiated/neural crest-like melanoma cell state and reduced in the MITFHI/melanocytic state. Increased DHRS3 expression is sufficient to drive MITFHI/melanocytic cells to a more undifferentiated/invasive state. These changes are due to retinoic acid-mediated regulation of melanocytic genes. Our data demonstrate that melanoma cell state can be regulated by expression of lipid droplet proteins which affect downstream retinoid signaling.

脂滴是一种脂肪储存细胞器,由蛋白质包膜和富含脂质的核心组成。对这种蛋白质包膜的调节是脂滴形成和功能差异的基础。在黑色素瘤中,脂滴的形成与肿瘤的进展和转移有关,但脂滴蛋白是否在其中发挥作用尚不清楚。为了解决这个问题,我们对黑色素瘤的脂滴包膜进行了蛋白质组学分析。我们发现,脂滴蛋白在不同的黑色素瘤状态(从黑色素细胞瘤到未分化瘤)中富集程度不同。DHRS3能将全反式视黄醛转化为全反式视黄醇,它在MITFLO/未分化/神经嵴样黑色素瘤细胞状态中上调,而在MITFHI/黑色素细胞状态中降低。DHRS3 表达的增加足以使 MITFHI/黑素细胞细胞进入未分化/侵袭状态。这些变化是由于视黄酸介导的黑色素细胞基因调控所致。我们的数据表明,黑色素瘤细胞的状态可以通过脂滴蛋白的表达来调节,而脂滴蛋白的表达会影响下游的视黄酸信号转导。
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引用次数: 0
UVA Irradiation Promotes Melanoma Cell Proliferation Mediated by OPN3 Independently of ROS Production. 紫外线照射促进黑色素瘤细胞增殖与 ROS 生成无关,由 OPN3 介导。
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-30 DOI: 10.1111/pcmr.13206
Yulei Zhang, Wen Zeng, Wei Zhang, Yu Wang, Shuqi Jin, Ting Liu, Huanhuan Luo, Hongguang Lu

UVA radiation, a primary risk factor in melanoma progression, partly acts through the mediation of reactive oxygen species (ROS). The role of ROS in driving cutaneous melanoma toward an invasive phenotype and whether it occurs through opsins (OPNs), which are photosensitive G protein-coupled receptors, is not fully understood. This study focuses on the impact of UVA radiation on melanoma cell proliferation, with a special emphasis on OPN3. Investigating the biphasic response to various UVA doses (0.75-9 J/cm2) in A375 and MV3 cell lines, and using EdU and CCK-8 assays, we observed dose-dependent changes in cell proliferation. Interestingly, UVA irradiation at these doses of 0.75, 1.5 and 3 J/cm2 did not significantly induce ROS production. Our study further delves into the role of OPN3, a photosensitive receptor, in melanoma progression. Following UVA exposure, an increase in OPN3 expression was observed in melanoma cells lines A375 and MV3, indicating its role as a UVA-sensitive sensor and its influence on cell proliferation. Additionally, UVA-induced calcium flux in two melanoma cells lines pointed to a calcium-dependent G protein-coupled pathway in melanoma proliferation, mediated by OPN3 and not reliant on ROS. This research sheds light on the mechanism of UVA-induced melanoma progression, underscoring OPN3 as a pivotal regulator and advancing our understanding of UVA's interaction with opsins in melanoma progression.

UVA 辐射是导致黑色素瘤恶化的主要风险因素,其部分作用是通过活性氧(ROS)来实现的。目前还不完全清楚 ROS 在促使皮肤黑色素瘤形成侵袭性表型方面所起的作用,以及这种作用是否是通过对光敏感的 G 蛋白偶联受体 opsins(OPNs)产生的。本研究重点关注 UVA 辐射对黑色素瘤细胞增殖的影响,并特别强调 OPN3。通过研究 A375 和 MV3 细胞系对不同 UVA 剂量(0.75-9 J/cm2)的双相反应,并使用 EdU 和 CCK-8 检测法,我们观察到细胞增殖的变化与剂量有关。有趣的是,0.75、1.5 和 3 J/cm2 剂量的 UVA 照射并没有显著诱导 ROS 的产生。我们的研究进一步探讨了光敏受体 OPN3 在黑色素瘤进展中的作用。暴露于 UVA 后,在黑色素瘤细胞系 A375 和 MV3 中观察到 OPN3 的表达增加,这表明它作为 UVA 敏感传感器的作用及其对细胞增殖的影响。此外,两种黑色素瘤细胞系中 UVA 诱导的钙通量表明,黑色素瘤增殖过程中的钙依赖性 G 蛋白偶联通路由 OPN3 介导,而不依赖于 ROS。这项研究揭示了 UVA 诱导黑色素瘤发展的机制,强调了 OPN3 是一个关键的调节因子,并加深了我们对 UVA 与黑色素瘤发展过程中的蛋白相互作用的理解。
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引用次数: 0
Bay 11-7082, an NF-κB Inhibitor, Prevents Post-Inflammatory Hyperpigmentation Through Inhibition of Inflammation and Melanogenesis. NF-κB 抑制剂 Bay 11-7082 可通过抑制炎症和黑色素生成来预防炎症后色素沉着。
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-27 DOI: 10.1111/pcmr.13207
Juwon Moon, Ik Jun Moon, Hoyong Hyun, Jae Min Yoo, Seung Hyun Bang, Youngsup Song, Sung Eun Chang

Post-inflammatory hyperpigmentation (PIH) is a very common disorder of cutaneous hyperpigmentation, which poses a persistent management challenge in the fields of dermatology and esthetics. This study was designed to explore the anti-melanogenic and anti-inflammatory effects of Bay 11-7082, an NF-κB inhibitor, using small-molecule screening, to determine its potential application for PIH prevention. The molecular mechanisms were investigated in vitro and ex vivo in epidermis-humanized mice using melanin content, RT-PCR, and immunoblotting. Bay 11-7082 suppressed proinflammatory cytokines and ameliorated 2,4-dinitrofluorobenzene (DNFB)-induced contact dermatitis on day 15. The suppression of melanin synthesis by Bay 11-7082 was attributed to the reduction of MITF, which was induced by extracellular signal-regulated kinase activation. Bay 11-7082 reduced epidermal melanin accumulation in UVB-stimulated ex vivo human epidermis as well as in the ear and tail skin of K14-stem cell factor (SCF) transgenic mice. Topical administration of Bay 11-7082 improved PIH on day 35 in the post-DNFB dorsal skin of K14-SCF transgenic mice. In conclusion, Bay 11-7082 can be considered a promising candidate for the development of a preventive topical agent for PIH.

炎症后色素沉着(PIH)是一种非常常见的皮肤色素沉着疾病,在皮肤病学和美容领域一直是一个管理难题。本研究旨在通过小分子筛选,探索一种 NF-κB 抑制剂 Bay 11-7082 的抗黑色素生成和抗炎作用,以确定其在预防 PIH 方面的潜在应用。研究人员利用黑色素含量、RT-PCR 和免疫印迹技术,对表皮人源化小鼠的体外和体内分子机制进行了研究。Bay 11-7082抑制了促炎细胞因子,并在第15天改善了2,4-二硝基氟苯(DNFB)诱导的接触性皮炎。Bay 11-7082 抑制黑色素合成的原因是细胞外信号调节激酶活化诱导的 MITF 减少。Bay 11-7082 可减少 UVB 刺激的体外人体表皮以及 K14 干细胞因子(SCF)转基因小鼠耳部和尾部皮肤的表皮黑色素积累。外用 Bay 11-7082 在第 35 天改善了 K14-SCF 转基因小鼠 DNFB 后背侧皮肤的 PIH。总之,Bay 11-7082 可被视为开发 PIH 预防性局部用药的理想候选药物。
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引用次数: 0
Low-Dose Baricitinib Plus Narrow-Band Ultraviolet B for the Treatment of Progressive Non-Segmental Vitiligo: A Prospective, Controlled, Open-Label Study. 低剂量巴利替尼加窄带紫外线 B 治疗进展期非节段性白癜风:一项前瞻性、对照、开放标签研究。
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-23 DOI: 10.1111/pcmr.13209
Zhonghui Hu, Lu Lu, Jindi Feng, Hongbin Song, Shiyu Zhang, Lu Yang, Yuehua Liu, Tao Wang

Vitiligo is a chronic autoimmune disease, and current treatments for vitiligo have limited efficacy. Janus kinase (JAK) inhibitors could offer new therapeutic options. To evaluate the efficacy and safety of baricitinib, an oral JAK1/2 inhibitor, combined with narrow-band ultraviolet B (NB-UVB) in vitiligo treatment. This prospective, controlled, open-label study included adults with progressive non-segmental vitiligo (NSV). Patients were assigned to combination therapy with baricitinib 2 mg daily and NB-UVB three times a week or NB-UVB alone three times a week (control). The primary endpoint was the proportion of patients achieving 50% or greater improvement from baseline in the total Vitiligo Area Scoring Index (T-VASI50) at week 16. Of the 33 patients (mean age, 34.1 years; 27.3% women) who completed the study, 12 of 17 (70.6%) patients in the combination group and 2 of 16 (12.5%) in the control group had a T-VASI50 response at week 16 (relative risk [RR] = 5.6; 95% CI = 1.5-21.4; p = 0.001). Adverse events were minor, including erythema, mild blister after phototherapy and acne. Combination therapy with low-dose baricitinib and NB-UVB was effective and well tolerated in adults with progressive NSV.

白癜风是一种慢性自身免疫性疾病,目前治疗白癜风的方法疗效有限。Janus激酶(JAK)抑制剂可提供新的治疗选择。目的是评估口服JAK1/2抑制剂巴利昔尼(baricitinib)联合窄带紫外线B(NB-UVB)治疗白癜风的疗效和安全性。这项前瞻性、对照、开放标签研究纳入了进展期非节段性白癜风(NSV)成人患者。患者被分配接受巴利昔尼(baricitinib)每天2毫克、NB-UVB每周三次的联合治疗,或仅接受NB-UVB每周三次的治疗(对照组)。主要终点是在第16周时,白癜风总面积评分指数(T-VASI50)比基线提高50%或以上的患者比例。在完成研究的 33 名患者(平均年龄 34.1 岁;27.3% 为女性)中,联合用药组 17 名患者中有 12 名(70.6%)在第 16 周时对 T-VASI50 有反应,对照组 16 名患者中有 2 名(12.5%)(相对风险 [RR] = 5.6;95% CI = 1.5-21.4;P = 0.001)。不良反应较轻,包括红斑、光疗后轻度水疱和痤疮。小剂量巴利昔尼和NB-UVB联合疗法对进展期NSV成人患者有效且耐受性良好。
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引用次数: 0
25th Annual meeting of the European Society for Pigment Cell Research, Marseille, France 第 25 届欧洲色素细胞研究学会年会,法国马赛
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13192
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引用次数: 0
PASPCR 2024 Annual Meeting, New York, NY PASPCR 2024 年年会,纽约州纽约市
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-14 DOI: 10.1111/pcmr.13191
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引用次数: 0
Meeting Report From the 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Philadelphia, PA, November 2023. 2023 年治疗眼部黑色素瘤(CURE OM)全球科学会议报告,宾夕法尼亚州费城,2023 年 11 月。
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-09 DOI: 10.1111/pcmr.13205
Rino S Seedor, Andrew E Aplin, Corine Bertolotto, Richard D Carvajal, Nigel Deacon, Katie Doble, Omid Hamid, Rizwan Haq, Miriam Kadosh, Shaheer Khan, Jacqueline Kraska, Jose Lutzky, Meredith McKean, Kamaneh Montazeri, Justin Moser, Michael Onken, Marlana Orloff, Joseph J Sacco, Keiran Smalley, Sara M Selig

The 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting was held in Philadelphia on November 6, 2023. There is increased awareness and dedicated research in uveal melanoma (UM), but unmet needs remain in the prevention, detection, and treatment of UM. The purpose of this meeting was to provide an international forum for the exchange of research ideas, to allow for discussion of basic science as well as clinical research on UM, and to gather input about advocacy and patient needs.

2023 年眼部黑色素瘤(CURE OM)全球科学会议于 2023 年 11 月 6 日在费城举行。人们对葡萄膜黑色素瘤(UM)的认识不断提高,研究也越来越深入,但在 UM 的预防、检测和治疗方面仍有许多需求尚未得到满足。本次会议的目的是提供一个交流研究想法的国际论坛,允许讨论基础科学以及 UM 的临床研究,并收集有关宣传和患者需求的意见。
{"title":"Meeting Report From the 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting, Philadelphia, PA, November 2023.","authors":"Rino S Seedor, Andrew E Aplin, Corine Bertolotto, Richard D Carvajal, Nigel Deacon, Katie Doble, Omid Hamid, Rizwan Haq, Miriam Kadosh, Shaheer Khan, Jacqueline Kraska, Jose Lutzky, Meredith McKean, Kamaneh Montazeri, Justin Moser, Michael Onken, Marlana Orloff, Joseph J Sacco, Keiran Smalley, Sara M Selig","doi":"10.1111/pcmr.13205","DOIUrl":"https://doi.org/10.1111/pcmr.13205","url":null,"abstract":"<p><p>The 2023 Cure Ocular Melanoma (CURE OM) Global Science Meeting was held in Philadelphia on November 6, 2023. There is increased awareness and dedicated research in uveal melanoma (UM), but unmet needs remain in the prevention, detection, and treatment of UM. The purpose of this meeting was to provide an international forum for the exchange of research ideas, to allow for discussion of basic science as well as clinical research on UM, and to gather input about advocacy and patient needs.</p>","PeriodicalId":219,"journal":{"name":"Pigment Cell & Melanoma Research","volume":null,"pages":null},"PeriodicalIF":3.9,"publicationDate":"2024-10-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142386801","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
Sex Differences in Acral Lentiginous Melanoma: A Retrospective Cohort Analysis of 3617 Cases From the Surveillance, Epidemiology, and End Results Database. 口腔扁平状黑色素瘤的性别差异:对监测、流行病学和最终结果数据库中 3617 例病例的回顾性队列分析。
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-10-01 DOI: 10.1111/pcmr.13200
Jennifer M Fernandez, Mitchell A Taylor, Katherine Plampton, Erin X Wei, Ashley Wysong
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引用次数: 0
LL37-DNA Complex Drives Vitiligo Progression Through TLR9-MyD88 Signaling Pathways. LL37-DNA复合物通过TLR9-MyD88信号通路驱动白癜风进展
IF 3.9 3区 医学 Q2 CELL BIOLOGY Pub Date : 2024-09-30 DOI: 10.1111/pcmr.13202
Jingying Wang, Hanxiao Mao, Rulan Liu, Ziyuan Zeng, Lvsha Xie, Yan Yang, Yuanmin He

Vitiligo is an autoimmune disorder characterized by chronic depigmentation and milk-white patches on the skin. Skin infiltration by autoreactive CD8+ T cells causes melanocyte destruction in vitiligo. Multiple risk factors, particularly immune-related inflammatory factors, are involved in the disappearance of melanocytes. LL37 is a classic damage-associated molecular pattern molecule that is involved in the development of various autoimmune diseases. An enhanced expression of LL37 in vitiligo is known; however, the exact role of LL37 in melanocyte loss has not yet been elucidated. In the present study, we detected increased LL37 expression in vitiligo serum and lesions. Furthermore, we confirmed that cultured keratinocytes released LL37 after treatment with H2O2. Moreover, the LL37-DNA complex enhanced the secretion of CXCL9, CXCL10, and CXCL16 from keratinocytes via the TLR9-MyD88 signaling pathway and facilitated the migration of CD8+ T cells. Altogether, our study demonstrates that LL37 released from keratinocytes binds to DNA and contributes to melanocyte destruction under oxidative stress-induced autoimmunity in vitiligo.

白癜风是一种自身免疫性疾病,其特征是皮肤上出现慢性色素脱失和乳白色斑块。自体反应性 CD8+ T 细胞对皮肤的浸润导致白癜风患者黑色素细胞的破坏。黑色素细胞的消失涉及多种危险因素,尤其是与免疫相关的炎症因素。LL37 是一种典型的损伤相关分子模式分子,与各种自身免疫性疾病的发生有关。众所周知,LL37 在白癜风中的表达增强;然而,LL37 在黑色素细胞脱失中的确切作用尚未阐明。在本研究中,我们检测到 LL37 在白癜风血清和皮损中的表达增加。此外,我们还证实培养的角质细胞在经 H2O2 处理后会释放 LL37。此外,LL37-DNA 复合物通过 TLR9-MyD88 信号通路增强了角朊细胞分泌的 CXCL9、CXCL10 和 CXCL16,并促进了 CD8+ T 细胞的迁移。总之,我们的研究表明,在氧化应激诱导的白癜风自身免疫作用下,从角质形成细胞释放的LL37可与DNA结合并导致黑色素细胞破坏。
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引用次数: 0
Cholinergic Signaling Mediated by Muscarinic Receptors Triggers the Ultraviolet-Induced Release of Melanosome in Cultured Melanoma Cells. 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 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

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.

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。
{"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":"https://doi.org/10.1111/pcmr.13201","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":3.9,"publicationDate":"2024-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"142338012","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":3,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
引用次数: 0
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Pigment Cell & Melanoma Research
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