刺
干扰素基因刺激剂
CXCL10型
趋化因子
伤口愈合
干扰素
促炎细胞因子
刺激
CXCR3型
药理学
信号转导
医学
免疫学
炎症
细胞生物学
生物
免疫系统
先天免疫系统
内科学
工程类
航空航天工程
趋化因子受体
作者
Yuki Mizutani,Ayumu Kanbe,Hiroyasu Ito,Mariko Seishima
标识
DOI:10.1016/j.jdermsci.2019.11.008
摘要
Abstract
Background
The process of repair after skin injury is precisely regulated by a variety of mediators such as cytokines and chemokines. Recent reports demonstrated that cytoplasmic DNA-sensor cyclic GMP-AMP synthase (cGAS) activates the stimulator of interferon genes (STING) via production of cyclic GMP-AMP (cGAMP) and subsequently induces inflammatory cytokines, including type I interferon (IFN). Objective
We examined whether activation of the STING pathway by cGAMP affects the process of skin wound repair. Methods
The skin wound repair model was established using wild-type (WT) mice. Two full-thickness skin biopsies were taken from the right and left subscapular regions. One site was treated with ointment containing cGAMP, and the other was treated with a control ointment. Changes in wound size over time were calculated using photography. Results
Treatment with cGAMP significantly accelerated skin wound healing up to day 6. Biochemical analyses showed that topical treatment with cGAMP on wound sites promoted STING signaling pathway and enhanced the expression of IFN-β, CXCL10 and CCL2 in the wound sites treated with cGAMP markedly compared with the control. The scratch assay also revealed that cGAMP treatment accelerated wound closure in mouse embryonic fibroblasts. The acceleration of skin wound repair by cGAMP in WT mouse was impaired by administration of anti-IFNR antibody and anti-CXCR3 antibody respectively. Conclusion
These results revealed that topical treatment with cGAMP accelerates skin wound healing by inducing type I IFN and CXCL10/CXCR3. Topical administration of cGAMP might contribute to new effective treatments for accelerating skin wound healing.
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