伤口愈合
泛素连接酶
炎症
转化生长因子
细胞生物学
信号转导
生长因子
泛素
转化生长因子β
生物
癌症研究
免疫学
化学
基因
受体
生物化学
作者
Christina H. Stuelten,Nicolas Melis,Bhagawat C. Subramanian,Yi Tang,Megan Kimicata,John P. Fisher,Roberto Weigert,Ying E. Zhang
标识
DOI:10.1016/j.ajpath.2022.08.002
摘要
Wound healing is a highly conserved process that restores the integrity and functionality of injured tissues. Transforming growth factor (TGF)-β is a master regulator of wound healing, whose signaling is attenuated by the E3 ubiquitin ligase Smurf2. Herein, the roles of Smurf2 in cutaneous wound healing were examined using a murine incisional cutaneous model. Loss of Smurf2 increased early inflammation in the wounds and led to narrower wounds with greater breaking strength. Loss of Smurf2 also led to more linearized collagen bundles in normal and wounded skin. Gene expression analyses by real-time quantitative PCR indicated that Smurf2-deficient fibroblasts had increased levels of TGF-β/Smad3 signaling and changes in expression profile of genes related to matrix turnover. The effect of Smurf2 loss on wound healing and collagen bundling was attenuated by the heterozygous loss of Smad3. Together, these results show that Smurf2 affects inflammation and collagen processing in cutaneous wounds by down-regulating TGF-β/Smad3 signaling.
科研通智能强力驱动
Strongly Powered by AbleSci AI