Figure 3.
Hypoxia- and low temperature–induced transferrin upregulation to potentiate enzymatic activities of thrombin and FXIIa. (A-D,G-J) Effects of anti–Tf-AB, IgG control, RNR-Tf virus, blank (RNR) virus, and HIF inhibitor LW6, on HIF-1α and transferrin expression in liver or transferrin expression in plasma of mice following hypoxia and low-temperature treatment was determined by western blotting (A-C,G-I) or ELISA (D,J) (n = 6-7). (E-F,K-L) Relative activities of thrombin (E and K) and FXIIa (F,L) in plasma were examined (n = 6-7). β-actin was used as loading control in panels A and G. Animal experiments were repeated 3 times, independently. Data represent mean ± SD. Each point represents 1 mouse. Panels B-F and H-L, ∗P < .05, ∗∗P < .01 by unpaired t test. Western blots were from different membranes, and representative blots are shown in panels A and G.

Hypoxia- and low temperature–induced transferrin upregulation to potentiate enzymatic activities of thrombin and FXIIa. (A-D,G-J) Effects of anti–Tf-AB, IgG control, RNR-Tf virus, blank (RNR) virus, and HIF inhibitor LW6, on HIF-1α and transferrin expression in liver or transferrin expression in plasma of mice following hypoxia and low-temperature treatment was determined by western blotting (A-C,G-I) or ELISA (D,J) (n = 6-7). (E-F,K-L) Relative activities of thrombin (E and K) and FXIIa (F,L) in plasma were examined (n = 6-7). β-actin was used as loading control in panels A and G. Animal experiments were repeated 3 times, independently. Data represent mean ± SD. Each point represents 1 mouse. Panels B-F and H-L, ∗P < .05, ∗∗P < .01 by unpaired t test. Western blots were from different membranes, and representative blots are shown in panels A and G.

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