Gp130 triggers fibroblast activation and tracheal fibrosis via the YAP/β-catenin pathway

Tracheal fibrosis is a key abnormal repair process that leads to fatal stenosis and is characterized by fibroblast overactivation and extracellular matrix (ECM) deposition. The protein Gp130 encoded by IL6ST is a signal sensor shared by a variety of cytokines including IL6, CNTF, LIF and OSM, and participate in the damage repair of various tissues, but its role in tracheal fibrosis is still unclear. This study investigated the potential role of IL6ST as a novel regulator of tracheal fibrosis. The results showed that the expressions of serum IL6, L27, OSM and Gp130 were significantly increased in patients with abnormally repaired after tracheal injury. In summary, our findings suggested that IL6ST may trigger fibroblast activation and cell proliferation in tracheal fibrosis via the YAP/β-catenin signaling pathway. Targeting IL6ST may be a promising approach for the treatment of tracheal fibrosis. <fig><object-id>erj;64/suppl_68/PA3507/F1</object-id><object-id>F1</object-id><object-id>F1</object-id><graphic></graphic></fig> Figure1 Expression levels of serum IL6, IL27, OSM and Gp130 in patients with tracheal fibrosis. <fig><object-id>erj;64/suppl_68/PA3507/F2</object-id><object-id>F2</object-id><object-id>F2</object-id><graphic></graphic></fig> Figure2 Overexpression of IL6ST in primary rat fibroblasts promotes ECM synthesis and activates the YAP/β-catenin pathway.