Fig. 5: Influence of pharmacological treatments on junction stability.
From: Feedback between mechanosensitive signaling and active forces governs endothelial junction integrity
a Transients in bound cadherin following altered RhoA or Rac1 signaling which underpins strong, weak, rupture/heal junctions or disconnected cells. Corresponding parameters shown on (b); Predicted (b) cell contractility and (c) polymerization induced stress in the phase space spanned by RhoA-associated feedback parameter \({\alpha }_{c}\) and Rac1-associated maximum polymerization stress \({\sigma }_{P0}\); (d) Phase diagram of junction behavior as driven by actin polymerization and adhesion-mediated feedback, showing bound cadherin density; (e) PREM images of HUVECs showing cytoskeleton organization and junction state associated with control conditions and treatment with Y-27632 or CK666. Contacting cells are pseudo-colored to highlight cell boundary, which was identified based on immunogold VE-cadherin labeling. Scale bars, 0.5 \(\mu m\); (f) Local intensity of cadherin (\(n=6\) junctions), actin (\(n=4\) (control), \(n=6\) (Y27632), \(n=5\) (CK666)), and protrusion area (\(n=4\) (control), \(n=4\) (Y27632), \(n=5\) (CK666))) along cell-boundaries in response to Y-27632 or CK-666 treatment (mean \(\pm\) s.e.m.); HUVEC adherens junctions showing (g) cadherin and (h) actin intensity over time in response to Y-27632 or CK-666 treatment. Scale bars, 1 \(\mu m\).
