To investigate the effect of Stanniocalcin-1 (STC1) on the proliferation of airway smooth muscle and explore the possible role of STC1 in the airway remodeling in the mice with chronic obstructive pulmonary disease (COPD).

COPD mice model was established by ozone (O₃) exposure. Twenty-four BALB/c female mice were randomly divided into four groups (n=6): 1-week control (1WC) group, 1-week O₃ exposed (1WO₃) group, 3-week control (3WC) group and 3-week O₃ exposed (3WO₃) group. Hematoxylin-eosin (HE) staining was employed to observe the pulmonary inflammation, the alveolar spacing and the basement membrane thickness. Immunohistochemistry technique was used to detect the expression of α-SMA and STC1 in the lung tissues of the mice. Simultaneously, human airway smooth muscle cells (HASMCs) were stimulated by 2% and 10% FBS, respectively. The HASMCs were then treated with recombinant STC1 (rhSTC1). The proliferation of HASMCs was detected by EdU staining.

O₃ exposure could induce pulmonary inflammation, emphysema and airway remodeling in the mice (basement membrane thickening and increased expression of smooth muscle cell marker α-SMA). Immunohistochemical analysis demonstrated that STC1 expression showed intense staining in the apical membrane of the bronchial epithelial cells and was increased in the O₃-exposed mice. However, with O₃ exposure for 3 weeks, the expression of STC1 in the lung tissues decreased compared with that of α-SMA. And rhSTC1 added the inhibition of the proliferation of smooth muscle cells.

STC1 expression in the bronchial epithelium can inhibit the proliferation of airway smooth muscle cells. Adequate STC1 administration may delay the occurrence of airway remodeling in the mice with COPD.