Figure 4.
Figure 4. Effect of PTX3 on the autocrine activity exerted by endogenous FGF2 in ECs. (A) Wounded BAE cell monolayers were grown in the absence (i) or in the presence (ii) of neutralizing anti-FGF2 antibodies (200 μg/mL) or PTX3 (666 nM) (iii). Microphotographs (original magnification, × 10) were taken 16 hours after wounding. White dotted lines mark the edge of the wound at the beginning of the experiment. (B) FGF2-T-MAE cells were seeded at 10 000 cells/cm2 in 24-well plates. After 24 hours, the medium was replaced without (ctrl) or with the addition of neutralizing anti-FGF2 antibody (αFGF2-Ab) (10 μg/mL), suramin (300 μM), PTX3 (222 nM), or CRP (222 nM). After 3 days the cells were counted and data were expressed as percentage of cell proliferation with respect to untreated controls. Each point is the mean ± SEM of 4 determinations in duplicate. Student t test, **P < .01.

Effect of PTX3 on the autocrine activity exerted by endogenous FGF2 in ECs. (A) Wounded BAE cell monolayers were grown in the absence (i) or in the presence (ii) of neutralizing anti-FGF2 antibodies (200 μg/mL) or PTX3 (666 nM) (iii). Microphotographs (original magnification, × 10) were taken 16 hours after wounding. White dotted lines mark the edge of the wound at the beginning of the experiment. (B) FGF2-T-MAE cells were seeded at 10 000 cells/cm2 in 24-well plates. After 24 hours, the medium was replaced without (ctrl) or with the addition of neutralizing anti-FGF2 antibody (αFGF2-Ab) (10 μg/mL), suramin (300 μM), PTX3 (222 nM), or CRP (222 nM). After 3 days the cells were counted and data were expressed as percentage of cell proliferation with respect to untreated controls. Each point is the mean ± SEM of 4 determinations in duplicate. Student t test, **P < .01.

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