Department of Clinical Molecular Medicine, Kobe University Graduate School of Medicine, Japan.
Exp Dermatol. 2010 Jul 1;19(7):654-60. doi: 10.1111/j.1600-0625.2010.01084.x. Epub 2010 Apr 20.
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.
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。