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Ultraviolet B Inhibits Skin Wound Healing by Affecting Focal Adhesion Dynamics
Author(s) -
Liu Han,
Yue Jiping,
Lei Qiang,
Gou Xuewen,
Chen ShaoYu,
He YuYing,
Wu Xiaoyang
Publication year - 2015
Publication title -
photochemistry and photobiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.818
H-Index - 131
eISSN - 1751-1097
pISSN - 0031-8655
DOI - 10.1111/php.12462
Subject(s) - wound healing , microbiology and biotechnology , adhesion , motility , focal adhesion , skin repair , keratinocyte , human skin , cytoskeleton , microtubule , cell adhesion , chemistry , biology , immunology , cell , in vitro , signal transduction , biochemistry , genetics , organic chemistry
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.