气道重塑是支气管哮喘的主要特征之一。研究表明GLCCI1与哮喘患者的糖皮质激素疗效密切相关，但其功能目前尚不清楚。我们前期研究发现，GLCCI1在支气管上皮细胞表达十分丰富，其在哮喘时表达降低，且GLCCI1基因敲除哮喘小鼠气道炎症、气道壁厚度及多种炎症因子如IL-13的表达较野生型明显。IL-13可通过诱导上皮细胞释放TGF-β参与气道重塑的形成，而骨膜蛋白作为IL-13的下游蛋白，可通过MMP-2和MMP-9途径激活TGF-β信号通路。据此，我们提出假说：GLCCI1可能通过IL-13/骨膜蛋白/TGF-β通路调控下游基因表达，在哮喘气道重塑中起保护作用。本研究拟利用支气管上皮细胞及GLCCI1敲除小鼠，以IL-13/骨膜蛋白/TGF-β通路为切入点，探讨GLCCI1在哮喘气道重塑中发挥的功能和作用。本研究将从GLCCI1这个新视点为揭示哮喘气道重塑的发生机制及防治提供新思路。

Airway remodeling is one of the main characteristics of bronchial asthma. Studies have shown that glucocorticoid-induced transcript 1 gene (GLCCI1) is closely related to the efficacy of glucocorticoids in asthmatic patients，but its function is not clear so far. Our previous studies have found that GLCCI1 is abundantly expressed in bronchial epithelial cells; GLCCI1 expression decreased in asthma; GLCCI1 knockout asthmatic mice showed more serious in airway inflammation and airway wall thickning, as well as a variety of inflammatory cytokines like IL-13. IL-13 is involved in the formation of airway remodeling by inducing the release of TGF-β from epithelial cells. As a downstream protein of IL-13, periostin activates TGF-β signaling through the MMP-2 and MMP-9 pathways. Accordingly, we hypothesize that GLCCI1 may regulate the IL-13 / periostin / TGF-β pathway and thus play a protective role in the airway remodeling of asthma. This study aims to investigate the role of GLCCI1 in airway remodeling of asthma by targeting the IL-13 / periostin / TGF-β pathway in both bronchial epithelial cell and GLCCI1 knockout mice. This study will provide a new idea from the new perspective of GLCCI1 to reveal the pathogenesis and prevention of airway remodeling in asthma.