Fig. 3From: Betulinic acid enhances TGF-β signaling by altering TGF-β receptors partitioning between lipid-raft/caveolae and non-caveolae membrane microdomains in mink lung epithelial cellsBetA enhances the TGF-β response downstream of ALK-5 in Mv1Lu cells. Cells stably expressing the PAI-1 luciferase promoter were transiently transfected with caALK-5 or pcDNA3.1 (as a control). These transfected cells exhibited a potent luciferase activity in the absence of exogenously added TGF-β. BetA appeared to enhance caALK-5-stimulated PAI-1 (a and b), fibronectin (c), and collagen (d) promoter luciferase expression in a concentration-dependent manner. Cholesterol treatment suppressed the BetA-enhanced luciferase activity. The data bar represents the mean ± SD from four different analyses. * and **Significantly higher than that in cells treated without BetA (a) or lower than that in cells treated without cholesterol (b, c, and d) (*: P < 0.05, **: P < 0.01)Back to article page