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. 2017 Sep 13;3(9):e1603259. doi: 10.1126/sciadv.1603259

Fig. 2. Effect of pharmacological inhibition or genetic deficiency of PAI-1 on the circulating levels of endogenous iFGF23 and clearance of rhFGF23 injected via the tail vein in mice with FA-induced AKI.

Fig. 2

(A) AKI induces plasma PAI-1 levels 10-fold higher in FA-treated WT mice (n = 13) compared to vehicle-treated WT mice (n = 5). (B) Mouse iFGF23 (miFGF23) levels in WT (n = 7), WT with AKI (n = 21), TM5441-treated WT with AKI (n = 15), PAI-1−/− with AKI (n = 9), and pai-1−/− untreated (n = 6). *P = 0.007, #P = 0.005. (C) Effect of PAI-1 inhibition on clearance of rhFGF23 in WT AKI mice (n = 7) and TM5441 (10 mg/kg per day)–treated WT AKI mice (n = 7). The rhFGF23 was injected into the tail vein, and human cFGF23 (hcFGF23) levels were measured in plasma samples collected at time points 1, 3, 5, 15, 30, 60, and 120 min. (D) The cFGF23 levels at 1 min were considered as 100% to plot percent remaining values of rhFGF23 over the time course of the experiment.