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Background：Abnormal proliferation, apoptosis, migration and contraction of airway smooth muscle (ASM) cells inairway remodeling in asthma are basical叹excessive repair responses to a network of inflammatory mediators suchas PDGF, but the mechanisms of such responses remain unclear. Nogo-B, a member of the reticulum family4(RTNa), is known to play a key role in arteriogenesis and tissue repair. Further studies are needed to elucidate therole of Nogo-B in airway smooth muscle abnormalities.Methods：A mouse model of chronic asthma was established by repented OVA inhalation and subjected to Nogo-Bexpression analysis using immunohistochemistry and Western Blotting. Then, primary human bronchial smoothmuscle cells (HBSMCs) were cultured in vitro and a siRNA interference was performed to knockdown the expressionof Nogo-B in the cells-The effects of Nogo-B inhibition on PDGF-induced IiBSMCs proliferation, migration andcontraction were evaluated-Finally, a protPOmic analysis was conducted to unveil the underlying mechanismsresponsible for the function of Nogo-B.Results：Total Nogo B expression was approximately 3.68 fold lower in chronic asthmatic mice compared to naivemice, which was obvious in the smooth musde layer of the airways. Interference of Nogo B expression饰siRNArexdted nearly％%reduction in mRNA in cultured HBSMCs. In addition, knockdown of Nogo-R using specificsiRNA significantly decreased PDGF-induced migrztion of HBSMCs by 2-3fold, and increased the cellularcontraction by 16Yo compared to negative controls, but had limited effects on PDGF induced proliferation.furthermore, using proteomic analysis, we demonstrate that the expression of actin related protein 7J3 complexsubunit 5 (ARPC 213) decreased and, myosin regulatory light chain 9 isoform a (MYL-9) increased after Nogo-Bknockdown.