Transforming growth factor beta-1 upregulates glucose transporter 1 and glycolysis through canonical and noncanonical pathways in hepatic stellate cells

Figure 5 The effect of glucose transporter 1 on the growth and proliferation of hepatic stellate cell. Mouse primary hepatic stellate cells (HSCs) were 1) pretreated with the glucose transporter 1 (GLUT1) inhibitor phloretin (50 μm) for 30 min and then treated with transforming growth factor-β1 (TGF-β1) (3 ng/mL) for 4 h or 2) transiently transfected with small interfering RNAs that inhibited GLUT1 expression, cultured in serum-free medium for 24 h and then treated with TGF-β1 (3 ng/mL) for 4 h. A: Cells were seeded in serum-free medium (4 × 10⁵ cells/well) in the upper chambers of a Transwell system. The lower chambers were filled with 5% glucose medium (700 μL per well). Changes in cell migration were observed. Representative images of crystal violet staining are shown; B: Quantitative data showing the number of migrating cells in each group; C: Western blot analysis using specific antibodies; D: Quantitative analysis of GLUT1 protein expression in three independent experiments; E: The effect of GLUT1 inhibition on the growth/proliferation of HSCs (mean ± SE; ^bP < 0.01 and ^cP < 0.001 compared with the group without TGF-β1; ^eP < 0.01 for the comparison of the TGF-β1-treated group with the groups subjected to TGF-β1 treatment and different interventions; Student’s t test). GLUT1: Glucose transporter 1; TGF-β1: Transforming growth factor-β1; siRNAs: Small interfering RNAs.