Fig. 4: EndoMT can be reverted by inhibiting TAK1.

a Confluent BECs were stimulated as indicated in the figure and as described in the materials and method section. Protein levels of phospho-TAK1 (Thr184/187) in cell lysates were determined by Western blot. Values were normalized to α-tubulin and plotted as fold change relative to control. b–e Stimulated-BECs were stained for NF-kB (p65 subunit) and analyzed using the A1R+ confocal resonant scanning laser microscope from Nikon (scale bar 20 µm). f NF-kB (p65 subunit) nuclear staining intensity was quantified using NIN ImageJ software analysis in three random fields in each well and is expressed as fold change intensity relative to unstimulated control cells. g mRNA expression levels of different EndoMT-related markers were determined by qRT-PCR upon stimulation of BECs. Values were normalized to GAPDH and plotted as fold change relative to control. h Nuclear protein content of SNAI1 was assessed by western blot and expressed as fold change compared to control cells. SnaI1 nuclear protein content was normalized using the nuclear envelope protein Lamin B. i, j The TEER (Rb, barrier resistance) and permeability to FITC-dextran (A.U. arbitrary unit) were measured and plotted as % of control BECs. Data presented are the mean of triplicate values ± SEM of three independent experiments. Statistical analysis was performed using one-way ANOVA where *p < 0.05, **p < 0.01, ***p < 0.001 with post-hoc Bonferroni correction