The Role and Effects of Glucocorticoid-Induced Leucine Zipper in the Context of Inflammation Resolution

摘要: Glucocorticoid (GC)-induced leucine zipper (GILZ) has been shown to mediate or mimic several actions of GC. This study assessed the role GILZ in self-resolving and GC-induced resolution neutrophilic inflammation induced by LPS mice. expression was increased during phase LPS-induced pleurisy, especially macrophages with resolving phenotypes. Pretreating LPS-injected mice trans-activator transcription peptide (TAT)-GILZ, a cell-permeable fusion protein, shortened intervals improved indices. Therapeutic administration TAT-GILZ resolution, decreased cytokine levels, promoted caspase-dependent neutrophil apoptosis. also modulated activation survival-controlling proteins ERK1/2, NF-κB Mcl-1. deficiency associated an early increase annexin A1 (AnxA1) did not modify course influx LPS. Dexamethasone treatment resolved that dependent on AnxA1. Dexamethasone-induced altered GILZ(-/-) due compensatory action Our results show therapeutic efficiently induces proapoptotic program promotes Alternatively, lack endogenous is compensated AnxA1 overexpression.