Loss of epidermal p38α signaling prevents UVR-induced inflammation via acute and chronic mechanisms.
Loss of epidermal p38α signaling prevents UVR-induced inflammation via acute and chronic mechanisms.
复制标题
DOI：
10.1038/jid.2014.153
复制
发表时间：
2014-08
影响因子：
6.5
通讯作者：
Park, Jin Mo
中科院分区：
文献类型：
--
作者：
Sano, Yasuyo;Park, Jin Mo
紫外线B辐射（UVB）是太阳辐射的一种成分，主要负责在受照射的皮肤中引起损伤和癌症，并破坏免疫稳态。过度阳光照射的直接危害和长期健康风险正在影响着全球几乎所有人的生活。炎症是UVB各种有害影响的关键机制。在这里，我们发现蛋白激酶p38α的激活仅限于UVB暴露皮肤的表皮，靶向上皮细胞的p38α消融足以抑制UVB诱导的炎症。从机制上讲，上皮p38α信号传导的缺失减弱了诱导血管渗漏和水肿所需的基因表达，并且还增加了表皮γδ T细胞的稳态丰度，已知其促进受损表皮的修复。p38α缺乏的这些影响描绘了在生物体-环境界面上运作的分子网络，并揭示了预防由阳光损伤皮肤引起的病理学的关键条件。
Ultraviolet B radiation (UVB) is a component of solar radiation primarily responsible for causing damage and cancer in irradiated skin, and disrupting immune homeostasis. The immediate harm and long-term health risks of excessive sunlight exposure are impacting the lives of nearly all people worldwide. Inflammation is a key mechanism underlying UVB’s various detrimental effects. Here we show that activation of the protein kinase p38α is restricted to the epidermis in UVB-exposed skin, and p38α ablation targeted to the epithelial compartment is sufficient to suppress UVB-induced inflammation. Mechanistically, loss of epithelial p38α signaling attenuates the expression of genes required to induce vascular leakage and edema, and also increases the steady-state abundance of epidermal γδ T cells, which are known to promote the repair of damaged epidermis. These effects of p38α deficiency delineate a molecular network operating at the organism-environment interface, and reveal conditions crucial to preventing the pathology resulting from sun-damaged skin.
登录
查看更多内容
影响因子：
64.5
作者：
FRESHNEY, NW;RAWLINSON, L;SAKLATVALA, J
通讯作者：
SAKLATVALA, J
DOI：
10.1126/stke.2003.167.re2
发表时间：
2003-01-28
期刊：
Science's STKE : signal transduction knowledge environment
影响因子：
--
作者：
Bode, Ann M;Dong, Zigang
通讯作者：
Dong, Zigang
影响因子：
5.3
作者：
Han, ZQS;Enslen, H;Ip, YT
通讯作者：
Ip, YT
影响因子：
9.2
作者：
Feldmeyer, Laurence;Keller, Martin;Beer, Hans-Dietmar
通讯作者：
Beer, Hans-Dietmar
影响因子：
5.3
作者：
Degols, G;Russell, P
通讯作者：
Russell, P