Figure 6

The release of LCN2 is reduced in Prkcd ^−/− mice in response to fMLP and cerebral ischemia. (A) Neutrophils from Prkcd ^+/+ and Prkcd ^−/− were stimulated with 1 μM of fMLP at 37°C for up to 120 min. LCN2 released into the media (release) and remained in neutrophils (PMN) at different time points were detected by western blot analysis. Actin detected in neutrophils (PMN) was used as the loading control. (B) Mouse sera collected at different time points after global cerebral ischemia were subjected to western blot analysis with anti-LCN2 and anti-IgG antibodies. The serum of mice without ischemia was collected as a control (0). The top panel is a representative western blot. The LCN2 and IgG protein bands were quantified by densitometry in the bottom panel. Ischemia-induced LCN2 differed by genotype [F(1,22) = 56.6; p < 0.0001] and time [F(3,22) = 60.5; p < 0.0001] with an interaction between these factors [F(3,22) = 21.3; p < 0.0001]. * p < 0.05 compared with time 0 within genotype. † p < 0.05 compared with Prkcd ^+/+ mice at the same time point (Bonferroni tests) (n = 3–5).