Fig. 2: Primary CF HBE cells show increased expression levels of mesenchymal markers and impaired TEER.
From: Mutant CFTR Drives TWIST1 mediated epithelial–mesenchymal transition
A Western blots showing epithelial (CFTR, CK18, ZO1, E-cadherin) and mesenchymal (N-cadherin, vimentin, αSMA) protein levels in fully differentiated Ctrl and CF (R347P/711 + 5 G > A) pHBE cells (21d of differentiation). In the R347P/711 + 5 G > A pHBE cells, a faint band C can still be seen for CFTR (arrowhead). GAPDH was used as a loading control. B Quantification by densitometry of the protein expression detected by WB in A. Data is normalized to loading control and showed as arbitrary units (A.U.), mean ± SEM. Asterisk indicates significant difference between Ctrl and CF pHBE cells (unpaired t-test, p < 0.05). The CF individuals’ genotypes were F508del/F508del, R347P/711 + 5 G > A and M1101K/1609delCA. (n = 3, unless indicated by (2)). C TEER measurements of CF and controls pHBE cells after 21 days in ALI. CF individuals’ genotypes were F508del/F508del, R347P/711 + 5 G > A and M1101K/1609delCA. Asterisk indicates significant difference between Ctrl and CF pHBE cells (unpaired t-test, p < 0.05). The number of filters used in the statistical analysis is indicated above each bar.
