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Published on: December 21, 2014
Fibrinogen Gamma Chain Mediates Airway Inflammation and Remodeling Through the Focal Adhesion and TGF-β/Smad2
Jiali Weng1, Hai Zhang1,2, Qing Chang1
1Department of Pulmonary and Critical Care Medicine, Shanghai Chest Hospital, Shanghai Jiao Tong University School of Medicine, NO.241, West Huaihai Road, Shanghai, 200030, People's Republic of China.
Background:
Chronic obstructive pulmonary disease (COPD) is a progressive disease characterized by chronic airway inflammation and remodeling. Fibrinogen gamma chain (FGG) has been implicated in the pathogenesis of multiple inflammatory and fibrotic conditions. However, the role and mechanisms of FGG in COPD remain unclear.
Methods:
FGG expression in lung tissues and plasma of COPD patients and CS-exposed mice was assessed. To investigate its functional role in cigarette smoke extract (CSE)-induced inflammation and epithelial-mesenchymal transition (EMT), we employed FGG knockdown (KD) and recombinant human FGG (rFGG) protein treatment in BEAS-2B cells and in a murine COPD model. To elucidate the related mechanisms in CSE-induced airway inflammation and EMT, BEAS-2B cells were treated with PF573228 (10 µM, a FAK inhibitor) or SB431542 (10 µM, a TGF-β type I receptor inhibitor).
Results:
FGG was up-regulated in both the lung tissue and plasma of COPD patients. Plasma FGG levels were negatively correlated with lung function in COPD patients. Similarly, elevated FGG expression was verified in CS-exposed mice and CSE-induced BEAS-2B cells. Both in vitro (FGG-KD in BEAS-2B) and in vivo (mouse model) experiments demonstrated that inhibition of FGG expression attenuated CSE-induced inflammatory cytokine release and EMT. Treatment with PF573228 or SB431542 inhibited airway inflammation and EMT, implicating the focal adhesion and TGF-β/Smad2 pathways.
Conclusions:
FGG contributes to airway inflammation and remodeling in COPD. Cigarette smoke enhances FGG expression and secretion in bronchial epithelium. Increased FGG promotes the release of inflammatory cytokines and EMT through the focal adhesion and TGF-β/Smad2 pathways.
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