Fig. 9

Knockdown of TGFBRII reduced LX2 cell activation. a Validation of siRNA knockdown efficiency of TGFBRII by qPCR. b Knockdown of TGFBRII inhibited the mRNA expression levels of TGFBRII, α-SMA and COLLAGEN I, determined by qPCR. c Knockdown of TGFBRII inhibited the protein expression levels of TGFBRII and profibrogenic protein (α-SMA, COLLAGEN I and KI67), detected by immunostaining. Red: TGFβRII. Green: Tubulin, COLLAGEN I, α-SMA and KI67. Blue: DAPI. (Original magnification, 20×, Scale bars, 40 μm). d Quantification of integrated optical density of proteins in c. e The capacity of cell proliferation was measured using cell viability assay with CCK8 kit in LX2 cells and TGFBRII KD LX2 cells treated with TGFβ or/and miR-6766-3p mimic. f Flow cytometry assay was performed to determine the changes of calcium content in LX2 cells and TGFBRII KD LX2 cells treated with TGFβ or/and miR-6766-3p mimic. g Quantification of cell cycle were measured by flow cytometry in LX2 cells and TGFBRII KD LX2 cells treated with TGFβ or/and miR-6766-3p mimic. h Quantification of wound recovery rates was modeled by cell scratch assays in LX2 cells and TGFBRII KD LX2 cells treated with different treatments, and the migration index was presented over time. (The images of cell scratch assays were provided in Additional file 1.). Data represent the mean ± SEM. *P < 0.05, **P < 0.01, and ***P < 0.001