Fig. 6.
Fig. 6. Effects of adenoviral-mediated IκB- expression on firm adhesion, transmigration, and rolling of monocytic cells on endothelial cells under physiological flow. HUVEC grown in 35-mm Petri dishes were left untreated (▩), were infected with rAd.IκB- (▪), or were infected with the control vector rAd.GFP encoding GFP (░). All cells were stimulated with TNF- (100 U/mL) for 4 hours. Mono Mac 6 cells were perfused at a constant flow rate of 1.5 dyn/cm2. (A) The firm, shear-resistant attachment of monocytes to HUVEC was determined by counting the number of cells firmly attached per field after a 5-minute period. (B) Cells undergoing shape change and spreading or transmigration were counted after 5 minutes and expressed as the percentage of cells initially attached. Data are the mean ± SD of three independent experiments. *P< .05 versus uninfected control.

Effects of adenoviral-mediated IκB- expression on firm adhesion, transmigration, and rolling of monocytic cells on endothelial cells under physiological flow. HUVEC grown in 35-mm Petri dishes were left untreated (▩), were infected with rAd.IκB- (▪), or were infected with the control vector rAd.GFP encoding GFP (░). All cells were stimulated with TNF- (100 U/mL) for 4 hours. Mono Mac 6 cells were perfused at a constant flow rate of 1.5 dyn/cm2. (A) The firm, shear-resistant attachment of monocytes to HUVEC was determined by counting the number of cells firmly attached per field after a 5-minute period. (B) Cells undergoing shape change and spreading or transmigration were counted after 5 minutes and expressed as the percentage of cells initially attached. Data are the mean ± SD of three independent experiments. *P< .05 versus uninfected control.

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