TLR3 activation induces S100A7 to regulate keratinocyte differentiation after skin injury  

作　　者：Hu Lei Yue Wang Tian Zhang Leilei Chang Yelin Wu Yuping Lai 

机构地区：[1]Shanghai Key Laboratory of Regulatory Biology, School of Life Sciences, East China Normal University, Shanghai 200241, China

出　　处：《Science China(Life Sciences)》2017年第2期158-167,共10页中国科学（生命科学英文版）

基　　金：supported by the National Natural Science Foundation of China (31170867, 31470878, 31222021,81202327);the Science and Technology Commission of Shanghai Municipality (13JC1402301, 11DZ2260300);Shanghai Education Commission (13SG25), and Henry Fok Educational Foundation (141017)

摘　　要：Human S100A7 (psoriasin) is highly expressed in psoriasis and other inflammatory diseases; however, the function of S100A7 in wound repair remains largely unknown. Here we demonstrated that skin injury increased the expression of S100A7. Damaged cells from wounded skin induced the expression of S100A7 via the activation of Toll-like receptor 3 (TLR3) followed by the activation of p38 MAPK. S100A7, in turn, acted on keratinocytes to induce the expression of terminal differentiation marker gene loricrin through the activation of p38 MAPK and caspase-1. The differentiation of keratinocytes induced by S100A7 resulted in skin stratification, thus efficiently promoting wound closure. Taken together, our results demonstrate that the activation of TLR3 accelerates wound closure via the induction of S100A7 to induce keratinocyte differentiation. These findings also provide new insights into the development of different forms of treatment with skin wounds.Human S 100A7 （psoriasin） is highly expressed in psoriasis and other inflammatory diseases; however, the function of S 100A7 in wound repair remains largely unknown. Here we demonstrated that skin injury increased the expression of S100A7. Damaged cells from wounded skin induced the expression of S100A7 via the activation of Toll-like receptor 3 （TLR3） followed by the activation of p38 MAPK. S100A7, in turn, acted on keratinocytes to induce the expression of terminal differentiation marker gene loricrin through the activation of p38 MAPK and caspase-1. The differentiation of keratinocytes induced by S100A7 resulted in skin stratification, thus efficiently promoting wound closure. Taken together, our results demonstrate that the activation of TLR3 accelerates wound closure via the induction of S100A7 to induce keratinocyte differentiation. These findings also provide new insights into the development of different forms of treatment with skin wounds.

关 键 词：TLR3 S100A7 CASPASE-1 keratinocyte differentiation wound closure 

分 类 号：R751[医药卫生—皮肤病学与性病学]