Potentiation of anti-angiogenic eNOS-siRNA transfection by ultrasound-mediated microbubble destruction in ex vivo rat aortic rings
Fig 5
Transfection of eNOS siRNA by MBs and UMMD efficiently inhibits NO production in bEnd.3 cells.
The upper panel (A) shows, representative confocal images depict endothelial NO release under different conditions: (a) Basal NO release; (b) Acetylcholine (Ach, 100 μM) stimulation; (c) Ach stimulation with NOS inhibitor L-NAME (1 mM); (e) Ach stimulation after transfection with eNOS-siRNA (42 ng)-MBs exposed to ultrasound (US); and (g) Ach stimulation after transfection with eNOS-siRNA (79 ng) using lipofectamine. NC-siRNA was used as a control for both UMMD and lipofectamine transfection (d and f, respectively). Quantification of fluorescence intensity (arbitrary units) of cells with or without Ach stimulation or treatment (control) is shown in panel (B). Each experimental condition was conducted in duplicate, and the entire experiment was replicated three times (n = 3). Data represent the mean ± standard error of the mean for three different experiments. *P ≤ 0.05 vs Ach.