Fig. 8.
Fig. 8. Angiostatin inhibits ERK1/2 phosphorylation induced by HGF but not by VEGF or bFGF. / (A) HUVECs in serum-free medium were stimulated with HGF (10 ng/mL) for 5 minutes with or without angiostatin at varying concentrations. Lane 1 is control (unstimulated cells); lane 2, HGF (10 ng/mL); lanes 3-6, HGF (10 ng/mL) plus angiostatin, at 0.5 μM (lane 3), 1.0 μM (lane 4), 2.0 μM (lane 5), and 3.0 μM (lane 6). (B) HUVECs in serum-free medium were unstimulated (lane 1) or treated with VEGF (50 ng/mL) in the absence (lane 2) or presence (lane 3) of angiostatin (ANG; 5 μM). Similarly, treatment with bFGF, 25 ng/mL (lane 4), resulted in ERK1/2 phosphorylation that was not inhibited by angiostatin (5 μM, lane 5).

Angiostatin inhibits ERK1/2 phosphorylation induced by HGF but not by VEGF or bFGF.

(A) HUVECs in serum-free medium were stimulated with HGF (10 ng/mL) for 5 minutes with or without angiostatin at varying concentrations. Lane 1 is control (unstimulated cells); lane 2, HGF (10 ng/mL); lanes 3-6, HGF (10 ng/mL) plus angiostatin, at 0.5 μM (lane 3), 1.0 μM (lane 4), 2.0 μM (lane 5), and 3.0 μM (lane 6). (B) HUVECs in serum-free medium were unstimulated (lane 1) or treated with VEGF (50 ng/mL) in the absence (lane 2) or presence (lane 3) of angiostatin (ANG; 5 μM). Similarly, treatment with bFGF, 25 ng/mL (lane 4), resulted in ERK1/2 phosphorylation that was not inhibited by angiostatin (5 μM, lane 5).

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