Figure 4.
Figure 4. Acetylsalicylic acid, piroxicam, and NS398 inhibited VEGF- and bFGF-induced CXCR4. (A-B) Regulation of COX by VEGF and bFGF. HMECs were stimulated with either bFGF (10 ng/mL) or VEGF (10 ng/mL) for 4 hours (A) or 18 hours (B); thereafter the levels of COX-1 and COX-2 were determined. (C-E) The basal expression of CXCR4-, VEGF-, or bFGF-induced CXCR4 in the presence (+) or absence (–) of aspirin (10–4 M) is shown. The isotype control is depicted by the dotted histograms. The data show one representative experiment of 3 performed. (F) Acetylsalicylic acid and NS398 inhibited VEGF- and bFGF-induced CXCR4 on HMECs. Treatment of HMECs with NS389 (1 μM), acetylsalicylic acid (10–4 M), piroxicam (1.5 μM) for 24 hours inhibited VEGF- and bFGF-mediated CXCR4 up-regulation. The results are expressed as the percentage of inhibition of CXCR4-induced expression after VEGF or bFGF stimulation. The data show mean + SEM of 3 experiments.

Acetylsalicylic acid, piroxicam, and NS398 inhibited VEGF- and bFGF-induced CXCR4. (A-B) Regulation of COX by VEGF and bFGF. HMECs were stimulated with either bFGF (10 ng/mL) or VEGF (10 ng/mL) for 4 hours (A) or 18 hours (B); thereafter the levels of COX-1 and COX-2 were determined. (C-E) The basal expression of CXCR4-, VEGF-, or bFGF-induced CXCR4 in the presence (+) or absence (–) of aspirin (10–4 M) is shown. The isotype control is depicted by the dotted histograms. The data show one representative experiment of 3 performed. (F) Acetylsalicylic acid and NS398 inhibited VEGF- and bFGF-induced CXCR4 on HMECs. Treatment of HMECs with NS389 (1 μM), acetylsalicylic acid (10–4 M), piroxicam (1.5 μM) for 24 hours inhibited VEGF- and bFGF-mediated CXCR4 up-regulation. The results are expressed as the percentage of inhibition of CXCR4-induced expression after VEGF or bFGF stimulation. The data show mean + SEM of 3 experiments.

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