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单纯疱疹病毒1型通过下调VN1R5/ERK途径抑制PIG1细胞的黑色素生成。

HSV-1 inhibits melanogenesis of PIG1 cells through downregulation of VN1R5/ERK pathway.

作者信息

Feng Yuxin, Jiang Shibin, Yuan Jinping, Zhou Kun, Lu Yansong, Zhuo Fenglin, Gao Xing-Hua, Chen Hong-Duo, Qi Rui-Qun, Wu Yan

机构信息

Department of Dermatology, The First Hospital of China Medical University, Shenyang, Liaoning, China.

Key Laboratory of Immunodermatology, Ministry of Education and NHC, National Joint Engineering Research Center for Theranostics of Immunological Skin Diseases, Shenyang, China.

出版信息

Arch Dermatol Res. 2025 Feb 6;317(1):347. doi: 10.1007/s00403-025-03844-5.

Abstract

Herpes simplex virus type 1 (HSV-1) is an ubiquitous pathogen that can infect humans through skin or mucous regions. This study was to explore the effects and underlying mechanism of HSV-1 as examined within the human epidermal melanocyte cell line, PIG1. Our results showed that following HSV-1 infection, PIG1 cells shrank and acquired a rounded shape, while the numbers and lengths of their dendrites decreased and melanogenesis was inhibited. Meanwhile, the HSV-1 receptors (nectin-1, herpes virus entry mediator, paired immunoglobulin-like type 2 receptor alpha) and phospho-extracellular signal-regulating kinase (p-ERK) were all substantially decreased, while vomeronasal type-1 receptor 5 (VN1R5) increased. Results of RNA interference and protein inhibitor assays revealed that knockdown of VN1R5 increased the expression of p-ERK and microphthalmia-associated transcription factor (MITF), while an inhibition of ERK decreased VN1R5 expression. Taken together, our study provides the first evidence that HSV-1 can infect human normal melanocytes and inhibit melanogenesis through VN1R5/ERK pathway.

摘要

单纯疱疹病毒1型(HSV-1)是一种普遍存在的病原体,可通过皮肤或黏膜区域感染人类。本研究旨在探讨HSV-1在人表皮黑素细胞系PIG1中的作用及其潜在机制。我们的结果表明,HSV-1感染后,PIG1细胞收缩并呈圆形,其树突的数量和长度减少,黑素生成受到抑制。同时,HSV-1受体(NECTIN-1、疱疹病毒进入介质、配对免疫球蛋白样2型受体α)和磷酸化细胞外信号调节激酶(p-ERK)均显著降低,而犁鼻器1型受体5(VN1R5)增加。RNA干扰和蛋白抑制剂检测结果显示,敲低VN1R5可增加p-ERK和小眼畸形相关转录因子(MITF)的表达,而抑制ERK可降低VN1R5的表达。综上所述,我们的研究首次证明HSV-1可感染人正常黑素细胞并通过VN1R5/ERK途径抑制黑素生成。

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