Figure 4.
Increased PAI-1 is not sufficient to explain delayed PG in HFD-fed mice. (A) Fibrinogen, (B) plasminogen, (C) α2-antiplasmin, (D) total PAI-1, and (E) active PAI-1 in plasma from CD- and HFD-fed mice. Fibrinogen was measured by immunoblot and densitometry to confirm presence of all 3 chains; β-chain was used for quantification. Plasminogen, α2-antiplasmin, and PAI-1 were measured by ELISA. (F-G) Correlation between total and active PAI-1 and body weight. (H-I) PG was measured in 1:3-diluted normal, pooled plasma triggered with 1 pM TF and 0.31 µg/mL rtPA in the presence of various concentrations of (H) total mouse and (I) conformationally active human PAI-1. Bars indicate medians. Each dot represents a separate mouse. NS, not significant.

Increased PAI-1 is not sufficient to explain delayed PG in HFD-fed mice. (A) Fibrinogen, (B) plasminogen, (C) α2-antiplasmin, (D) total PAI-1, and (E) active PAI-1 in plasma from CD- and HFD-fed mice. Fibrinogen was measured by immunoblot and densitometry to confirm presence of all 3 chains; β-chain was used for quantification. Plasminogen, α2-antiplasmin, and PAI-1 were measured by ELISA. (F-G) Correlation between total and active PAI-1 and body weight. (H-I) PG was measured in 1:3-diluted normal, pooled plasma triggered with 1 pM TF and 0.31 µg/mL rtPA in the presence of various concentrations of (H) total mouse and (I) conformationally active human PAI-1. Bars indicate medians. Each dot represents a separate mouse. NS, not significant.

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