Simvastatin Ameliorates Matrix Stiffness-Mediated Endothelial Monolayer Disruption
Fig 1
Simvastatin disrupts the RhoA pathway.
The Rho/Rho-associated kinase pathway activity is elevated in endothelial monolayers with increased matrix stiffness but is attenuated with 10 μM simvastatin treatment. (A) Bar graphs of RhoA-GTP activity in response to matrix stiffness and simvastatin treatment normalized to total protein of lysate (n = 2, performed in triplicate). (B) Representative Western blot probing for total cellular RhoA expression and alpha tubulin (α-tub) loading control. (C) Quantification of total RhoA normalized to alpha tubulin loading control demonstrating that RhoA expression is significantly increased by the simvastatin treatment (n = 5). (D) Representative Western blot probing for phosphorylated myosin light chain (pMLC) and alpha tubulin loading control. (E) Western blot quantification normalized to alpha tubulin loading control demonstrating simvastatin attenuates increased pMLC caused by increased substrate stiffness, (n = 4). Data are presented as means ± standard error of the mean, *p<0.05, **p<0.01, ***p<0.001 when compared to the untreated control at each stiffness.