Suppr超能文献

紫外线通过活性氧和 DNA 损伤诱导人角质形成细胞和成纤维细胞中 Stat3 的激活。

Ultraviolet light induces Stat3 activation in human keratinocytes and fibroblasts through reactive oxygen species and DNA damage.

机构信息

Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Japan.

出版信息

Exp Dermatol. 2010 Jul 1;19(7):654-60. doi: 10.1111/j.1600-0625.2010.01084.x. Epub 2010 Apr 20.

Abstract

Stat3 is activated by the outer stressors, such as ultraviolet (UV) exposure. In this study, we investigated the Stat3 response to UV irradiation in human epidermal keratinocytes and dermal fibroblasts. Results indicated that UVB and UVC differentially activate Stat3 in these cells. The UV-induced Stat3 activation was mediated by both reactive oxygen species (ROS) and DNA damage, and the dominancy of ROS and DNA damage to activate Stat3 depended on the wavelength of UV. By using fibroblasts from a patient with xeroderma pigmentosum A (XP-A) and those transfected with human XPA gene, we found that UVB activates Stat3 via both ROS and DNA damage, while UVC does so mainly via DNA damage. The present data suggest that Stat3 activation in UV-exposed human skin is one of the initial events where DNA damage and ROS are involved.

摘要

Stat3 被外部应激源激活,如紫外线 (UV) 照射。在这项研究中,我们研究了 Stat3 对人表皮角质形成细胞和真皮成纤维细胞中 UV 照射的反应。结果表明,UVB 和 UVC 在这些细胞中差异地激活 Stat3。UV 诱导的 Stat3 激活是由活性氧 (ROS) 和 DNA 损伤介导的,ROS 和 DNA 损伤对激活 Stat3 的主导作用取决于 UV 的波长。通过使用来自 XP-A 型着色性干皮病 (XP-A) 患者的成纤维细胞和转染人 XPA 基因的成纤维细胞,我们发现 UVB 通过 ROS 和 DNA 损伤激活 Stat3,而 UVC 主要通过 DNA 损伤激活 Stat3。本研究数据表明,暴露于 UV 下的人皮肤中的 Stat3 激活是涉及 DNA 损伤和 ROS 的初始事件之一。

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验