tPA and uPA participate in the delayed bleeding post-CHI. (A) Time course of tPA and uPA release post-CHI. The concentrations of tPA (filled squares) and uPA (empty squares) in the CSF of WT mice were measured by enzyme-linked immunosorbent assay before or at different time points after CHI. The mean ± SE of 3 experiments is shown (n = 3-7). (B) uPA mediates the delayed ICH in untreated mice. CHI was induced in WT mice. Thirty minutes or 8 hours postinjury, mice were given tPA-S⁴⁸¹A (1 mg/kg) or tranexamic acid (TA; 150 mg/kg). Twenty-four hours after CHI, brain hemoglobin was determined as in Figure 3B. The mean ± SD of 3 experiments performed is shown (n = 5-7). (C) The expression of uPA (upper row) and tPA (lower row) was measured in the brain parenchyma of WT mice without (time 0) or at specified times after CHI by western blot analysis. The lower panel shows expression of β-actin as a loading control. Data represent results from 1 of 3 independent experiments.