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. 2018 Dec 18;9:1810. doi: 10.3389/fphys.2018.01810

FIGURE 1.

FIGURE 1

Angiotensin II (AII) increased vascular smooth muscle cells (VSMCs) stiffness but had no effect on cell adhesion to anti-α5 antibody. Group average real-time recordings of cell stiffness (blue square), rupture events (green triangle), and rupture force (purple cross) for AII (n = 5t) treatment (A) and the addition of PBS (n = 10) (E). Average elastic modulus summed across all or 15 min of time points for the group of VSMCs before and after AII (10-6 M) treatment (B) (n = 5, p < 0.05) and PBS addition (F) (n = 10, p < 0.05). Average rupture numbers per curve summed across all or 15 min of time points for the group of VSMCs before and after addition of AII (C) (n = 5, p < 0.05) and PBS (G) (n = 10, p < 0.05). (D) Average rupture force summed across all or 15 min of time points for the group of VSMCs before and after addition of AII (D) (n = 5, p < 0.05) and PBS (H) (n = 10, p < 0.05). Data were collected by integrin α5 antibody coated AFM tip at 0.1 Hz of indentation frequency and are presented as mean ± SEM. tAs detailed in the text while eight cells were treated with AII analysis was limited to the five cells responding with the characteristic increase in cell stiffness as observed in previous studies.