Silencing of Gal-7 inhibits TGF-β1-induced apoptosis of human airway epithelial cells through JNK signaling pathway

Apoptosis of epithelial cells is regarded as the initial pathological process of many lung diseases, including asthma. Previous studies have identified that galectin-7 (Gal-7), a regulator of apoptosis, was overexpressed in bronchial epithelial cells in asthma. However, the effect and mechanism of Gal-7 in the progression of asthma is still unclear. In this study, we investigated the expression and role of Gal-7 in the apoptosis of bronchial epithelial cells BEAS-2B upon TGF-beta(1) stimulation. TGF-beta(1) significantly induced apoptosis of BEAS-2B cells, as determined by flow cytometry. Western blot results revealed that the mRNA and protein expression of Gal-7 were obviously increased after TGF-beta(1) stimulation. Small interfering RNA (siRNA)-mediated knockdown of Gal-7 abrogated TGF-beta(1) -evoked cell apoptosis. Simultaneously, increased Bcl-2 expression, decreased Bax expression and the cleavage of poly ADP-ribose polymerase (PARP) and caspase-3 activity were also monitored in TGF-beta(1) treated cells after Gal-7 sifINA transfection. Gal-7 silence also inhibited TGF-beta(1)-induced c-Jun N-terminal kinase (JNK) phosphorylation in BEAS-2B cells. Furthermore, anisomycin, a specific activator for JNK, reversed the effect of Gal-7 siRNA on cell apoptosis induced by TGF-beta(1). These results demonstrate that Gal-7 silence attenuates TGF-beta(1)-induced apoptosis in bronchial epithelial cells through the inactivation of JNK pathway. Therefore, Gal-7 may act as a potential target for asthma treatment.