Modulation of basal hydraulic stress through media osmolarity and substrate solute permeability regulate cell extrusion via FAK-Akt pathway.
(A) Cell extrusion rates on 100 μm waves in normal, sucrose, and sucrose + 3 μM FAKI14 media. (B) Adding 6 μM FAKI14 leads to cell death that compromised monolayers. Scale-bar: 50 μm. (C) Immunoblots of FAK and Akt proteins in MDCK cells subjected to treatments that lead to varying basal hydraulic stresses for 24 hours; namely, iso-osmotic (control), hyper-(4.1 wt. % sucrose), hypo- (25 % water), iso-osmotic with soft silicone and iso-osmotic with water/solute permeable PAM hydrogel. (D) and (E) Quantification of the relative expression levels of phosphorylated-FAK (tyr397) as a ratio of p-FAK to total FAK and phosphorylated-Akt (Ser473) as a ratio of p-Akt to total Akt, respectively. GAPDH was used as loading control (M ± SD, n = 5). Statistical analysis can be found in summary data in Supplementary File 8. (F) fluorescence images of cell nuclei (false blue), FAK (false red), and p-FAK at tyr397 (false green) on flat, hill and valley; the hill and valley images were unwrapped from 3D stacks. Scale-bar: 20 μm. (G) normalized p-FAK/FAK intensities from hill and valley cells. Statistical analysis can be found in summary data in Supplementary File 9. (H) and (I) Schematic of how osmolarity affect basal hydraulic stress and cell survival. (J) Schematic of how curvature induced force differences promote cell survival and death.