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

被引：33

作者：

Bito, Toshinori ^{[1
,2
]}

Sumita, Naoko ^{[2
]}

Masaki, Taro ^{[2
]}

Shirakawa, Toshiro ^{[3
]}

Ueda, Masato ^{[2
]}

Yoshiki, Ryutaro

Tokura, Yoshiki

Nishigori, Chikako ^{[2
]}

机构：

[1] Univ Occupat & Environm Hlth, Dept Dermatol, Yahatanishi Ku, Kitakyushu, Fukuoka 8078555, Japan

[2] Kobe Univ, Grad Sch Med, Dept Clin Mol Med, Div Dermatol, Kobe, Hyogo 657, Japan

[3] Kobe Univ, Grad Sch Med, Int Ctr Med Res & Treatment, Kobe, Hyogo 657, Japan

来源：

EXPERIMENTAL DERMATOLOGY | 2010年 / 19卷 / 07期

关键词：

DNA; reactive oxygen species; skin; Stat3; UV; CELL-LINES; CONSTITUTIVE ACTIVATION; IN-VIVO; SKIN; RADIATION; APOPTOSIS; CANCER; PROLIFERATION; INHIBITION; EXPRESSION;

D O I：

10.1111/j.1600-0625.2010.01084.x

中图分类号：

R75 [皮肤病学与性病学];

学科分类号：

100206 ;

摘要：

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.

引用

页码：654 / 660

页数：7

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