Induced global deletion of glucocorticoid receptor impairs fracture healing.

ABSTRACT: Although endogenous glucocorticoids (GCs) are important regulators of bone integrity and the immune system, their role in bone repair after fracture-a process highly dependent on inflammation and bone formation-is unclear. Because most effects of GCs are mediated by the glucocorticoid receptor (GR), we used an inducible global GR knockout (GR^{gtROSACreERT2}) mouse model to eliminate endogenous GC action in all cells contributing to bone repair. The healing process was analyzed by cytokine/chemokine multiplex analysis, flow cytometry, histology, gene-expression analysis, microcomputed tomography, and biomechanical analysis. We observed increased early systemic and local inflammatory responses, as well as a significantly higher number of T cells infiltrating the fracture callus. Lat

SUBMITTER: Rapp AE 

PROVIDER: S-EPMC5893166 | biostudies-literature | 2018 Apr

REPOSITORIES: biostudies-literature