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Fig. 2 | Journal of Biomedical Science

Fig. 2

From: 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 cells

Fig. 2

BetA enhances the transcriptional response stimulated by TGF-β in Mv1Lu cells. Cells stably expressing the PAI-1 luciferase reporter plasmid exhibited a 6-fold increase of the luciferase activity after stimulation with 100 pM TGF-β and the TGF-β-stimulated luciferase activity was enhanced by BetA in a concentration-dependent manner (a) and (b). However, the BetA-enhanced TGF-β-stimulated PAI-1 luciferase activity was diminished in the presence of cholesterol (b). Cells transiently transfected with the fibronectin (c) and collagen (d) luciferase reporter plasmids were treated with 100 pM TGF-β and increasing concentrations of BetA and/or cholesterol. BetA also enhanced the TGF-β-stimulated luciferase activity driven by the promoters of fibronectin (c) and collagen (d). The presence of cholesterol inhibited these BetA-enhanced luciferase activities (b, c, and d). The data bar represents the mean ± S.D. ** and * indicate the significant different between cells treated with or without BetA (a), or lower than that in cells treated without cholesterol in the same concentration of BetA group (b, c, and d) (*: P < 0.05, **: P < 0.01)

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