BACKGROUND: Asthma is a common chronic respiratory disease that influences 300 
million people all over the world. However, the pathogenesis of asthma has not 
been fully elucidated. It has been reported that transforming growth factor-β 
(TGF-β) can activate myofibroblasts. Moreover, the fibroblast to myofibroblast 
transformation (FMT) can be triggered by TGF-β, which is a major mediator of 
subepithelial fibrosis. Secreted modular calcium-binding protein 2 (SMOC2) is a 
member of cysteine (SPARC) family and is involved in the progression of multiple 
diseases. However, its role in asthma remains poorly understood. RT-qPCR 
evaluated the expression of SMOC2. Bromodeoxyuridine assay and wound-healing 
assay detected the proliferation and migration of lung fibroblasts, 
respectively. IF staining was performed to assess the expression of α-smooth 
muscle actin (α-SMA). Western blot analysis detected the levels of proteins. 
Flow cytometry was utilized for determination of the number of myofibroblasts.
RESULTS: We found the expression of SMOC2 was upregulated by the treatment of 
TGF-β1 in lung fibroblasts. In addition, SMOC2 promoted the proliferation and 
migration of lung fibroblasts. More importantly, SMOC2 accelerated FMT of lung 
fibroblasts. Furthermore, SMOC2 was verified to control the activation of AKT 
and ERK. Rescue assays showed that the inhibition of AKT and ERK pathway 
reversed the promoting effect of SMOC2 overexpression on proliferation, 
migration and FMT in lung fibroblasts.
CONCLUSIONS: This work demonstrated that SMOC2 modulated TGF-β1-induced 
proliferation, migration and FMT in lung fibroblasts and may promote asthma, 
which potentially provided a novel therapeutic target for the management of 
asthma.