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. 2010 Mar 18;285(21):15848–15857. doi: 10.1074/jbc.M109.075549

FIGURE 1.

FIGURE 1.

SphK1 prevents LPS-induced lung vascular hyper-permeability and edema formation. A, changes of microvessel permeability (measured as capillary filtration coefficient, Kf,c) in WT and SphK1−/− lungs in the presence and absence of LPS challenge (10 mg/kg, intraperitoneal). *, increase (p < 0.05) in Kf,c from basal value; **, increased (p < 0.05) Kf,c in SphK1−/− group compared with WT after LPS challenge. Results are mean of five independent experiments; bars indicate means ± S.E. B, time-dependent changes of pulmonary edema formation as measured by increase in wet weight of lungs of mice treated same as above. Lung wet weight was determined at the times indicated. *, increase (p < 0.05) in lung wet weight from basal value; **, increased (p < 0.05) lung wet weight in SphK1−/− group compared with WT after LPS challenge. Results are mean of 5 independent experiments; bars indicate means ± S.E. con, control. C, survival in mice after LPS (30 mg/kg, intraperitoneal) in WT and SphK1−/− mice (n = 20 each). Differences in mortality were assessed by log-rank test (p < 0.05).