Abstract
A previous study reported an elevated inflammation during tendon injury in mice with cystic fibrosis (CF), indicating the inadequate management of inflammation due to dysfunction of the cystic fibrosis transmembrane conductance regulator (CFTR). The objective of this study is to identify the targets of CFTR that contribute to the abnormal inflammation during tendon injury. A 2D gel electrophoresis and mass-spectrometry-based comparative proteomics is performed to find the molecular targets of CFTR. And the targeted protein is further confirmed at both mRNA and protein levels. It is identified that 14 proteins are differentially expressed, with annexin A1 being one of the most significantly downregulated protein. Further confirmation shows that annexin A1 is significantly decreased in TDSCs isolated from DF508 mice. As an essential anti-inflammation mediator, it is also downregulated in the injured tendon tissue of DF508 mice when compared with WT mice. Decreased annexin A1 expression can contribute to the elevated inflammation in DF508 mice during tendon injury. Therefore, annexin A1 can be considered as a new potential biomarker or drug target for a possible therapeutic approach in clinical practice.
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