Liu Han, Yue Jiping, Lei Qiang, Gou Xuewen, Chen Shao-Yu, He Yu-Ying, Wu Xiaoyang
Ben May Department for Cancer Research, The University of Chicago, Chicago, IL.
Section of Dermatology, Department of Medicine, The University of Chicago, Chicago, IL.
Photochem Photobiol. 2015 Jul-Aug;91(4):909-16. doi: 10.1111/php.12462. Epub 2015 May 16.
As the most important interface between human body and external environment, skin acts as an essential barrier preventing various environmental damages, among which DNA-damaging UV radiation from the sun remains the major environmental risk factor causing various skin diseases. It has been well documented that wavelengths in the ultraviolet B (UVB) radiation range (290-320 nm) of the solar spectrum can be absorbed by skin and lead to cutaneous injury and various other deleterious effects. During process such as wound healing, the orchestrated movement of cells in a particular direction is essential and highly regulated, integrating signals controlling adhesion, polarity and the cytoskeleton. Cell adhesion and migration are modulated through both of actin and microtubule cytoskeletons. However, little was known about how UVB affects skin wound healing and migration of epidermal keratinocytes. Here, we demonstrate that UVB can delay the wound healing progress in vivo with a murine model of full-thickness skin wound. In addition, UVB significantly inhibited keratinocyte motility by altering focal adhesion turnover and cytoskeletal dynamics. Our results provide new insights into the etiology of UVB exposure-induced skin damages.
作为人体与外部环境之间最重要的界面，皮肤起着至关重要的屏障作用，防止各种环境损害，其中来自太阳的DNA损伤性紫外线辐射仍然是导致各种皮肤病的主要环境风险因素。已有充分的文献记载，太阳光谱中紫外线B（UVB）辐射范围（290 - 320纳米）的波长可被皮肤吸收，并导致皮肤损伤和各种其他有害影响。在伤口愈合等过程中，细胞在特定方向上的协调运动至关重要且受到高度调节，整合了控制黏附、极性和细胞骨架的信号。细胞黏附和迁移通过肌动蛋白和微管细胞骨架进行调节。然而，关于UVB如何影响皮肤伤口愈合和表皮角质形成细胞迁移知之甚少。在这里，我们用全层皮肤伤口的小鼠模型证明，UVB可在体内延迟伤口愈合进程。此外，UVB通过改变粘着斑周转和细胞骨架动力学显著抑制角质形成细胞的运动性。我们的结果为UVB暴露引起的皮肤损伤的病因提供了新的见解。
