Fig. 1

Knockdown of FKBP10 reduces migration and adhesion of phLF. a Western Blot analysis of phLF treated with scrambled siRNA as control (sc) or FKBP10 siRNA (kd) and 2-phosphoascorbate (0.1 mM) in absence and presence of TGF-β1 (2 ng/mL) for 48h. Densitometric analysis and representative blots show the effect of FKBP10 knockdown on the expression of FKBP10 relative to β-actin as loading control (ACTB). b Quantitative reverse transcriptase-polymerase chain reaction analysis of phLF treated with sc siRNA as control or FKBP10 siRNA (kd) and 2- phosphoascorbate (0.1 mM) in absence and presence of TGF-β1 (2 ng/mL) for 48h. Transcript levels are shown as -ΔCt values. DEAH (Asp-Glu-Ala-His) Box Polypeptide 8 (DHX8) was used as endogenous control. Data (a, b) is based on eight independent experiments. c Representative images of a scratch assay of phLF treated with sc siRNA as control or FKBP10 and 2- phosphoascorbate (0.1 mM) in absence or presence of TGF-β1 (2 ng/mL). Images were taken at 0h and after 24h. d Analysis of open wound areas as shown in (c) normalized to controls at 0h (100%), given in % of the remaining wound area. Data is based on four independent experiments. e SCM assay of phLF treated with sc siRNA as control or FKBP10 siRNA and 2- phosphoascorbate (0.1 mM) in absence and presence of TGF-β1 (2 ng/mL). Cells were tracked over a period of 12h - 24h. Results of five independent experiments are shown as mean velocity of around 80 tracked cells per condition. f Cell attachment assay of phLF treated with sc siRNA as control or FKBP10 siRNA in absence or presence of TGF-β1 (2 ng/mL) for 48h. Results originate from six independent experiments and are visualized as percentage of cell adhesion normalized to non TGF-β1-treated cells. Statistical significance between control and FKBP10 kd is indicated by horizontal brackets and asterisks