원문정보
초록
영어
Posterior capsular opacification (PCO) is caused by the proliferation, migration, and epithelial-mesenchymal transition (EMT) of the human lens epithelial (HLE) cells after cataract surgery. GM3, modulating interactions and migration plays major roles in living organisms. So, we investigated correlation with GM3 and TGFβ receptor, a key regulator during PCO, in the HLE B-3 cells. Our results indicate that TLC data and immuno-fluorescence shows the increase of GM3 and GM2 during EMT induced by TGF-β1 in HLE B-3 cells. The expression of fibronectin, known as an EMT maker, at the mRNA level is controlled by expression of GM3 synthase in evidence of a dose- and time-dependent manner. GD3 synthase, downstream of GM3, and alpha-SMA did not change, however. GM3-depleting agents and siRNA of GM3 synthase specifically inhibited TGF-β–induced activation of fibronectin, TGFβR and Smad-2/3 compare as treatment of TGF-β1 only. Also, GM3 regulated TGF-β–promoted cell migration in HLE B-3 cells. Furthermore, TGF-β1 also increased binding between GM3 and TGFβ receptor detected by immune-precipitation. These results suggest that GM3, which is interacted with TGFβ receptor potentially, regulates the EMT in the human lens epithelial cells.