Inhibition of TGF-β1 Signaling by IL-15: A Novel Role for IL-15 in the Control of Renal Epithelial-Mesenchymal Transition: IL-15 Counteracts TGF-β1-Induced EMT in Renal Fibrosis
Figure 3
rhTGF-β1-induced EMT in RPTEC and HK-2 cells is inhibited by in vitro rhIL-15 treatment. (a) Analysis of E-cadherin and N-cadherin expressions in 48h-treated HK-2 cells by Western blotting using increasing concentrations of rhIL-15 (0.1-10 ng/mL) ± 3 ng/mL of rhTGF-β1. ( p<0.05, n=4, ±SEMs). (b) The same experiment was realized on RPTEC cells using 1 ng/mL of rhIL-15 and 3 ng/mL of rhTGF-β1 for 48h. Bar charts represent E-cadherin and N-cadherin expression normalized to β-actin (p<0.05, n=4, ±SEMs). (c) Fluorescent immunostaining for the epithelial markers E-cadherin and ZO-1 and the mesenchymal marker vimentin, under “spontaneous EMT” culture conditions. Cells were treated for 48h with rhTGF-β1 (3 ng/mL) ± rhIL-15 (1 ng/mL). In left panels, cells were viewed using phase contrast microscopy. Original magnification ×63. These data are representative of three independent experiments.