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. Author manuscript; available in PMC: 2017 Feb 1.
Published in final edited form as: Arterioscler Thromb Vasc Biol. 2016 Jan 7;36(2):380–388. doi: 10.1161/ATVBAHA.115.306997

Figure 3.

Figure 3

Loss of miR150−/− impairs resolution of vascular injury and increases sepsis mortality. A, Lung wet-dry ratio (left) and transendothelial albumin influx (EBAE) from lungs or plasma (right) were quantified after exposing indicated mice to nebulized (1 mg/ml) LPS (n=4–5). B, Mice were challenged with LPS (i.p, 40 mg/kg body weight) (left) or CLP was induced (right). n=10. C–D, WT-mice were exposed to nebulized (1 mg/ml) LPS and lungs were harvested to quantify alteration in miR-150–5p (left) or pri-miR-150 (right) (n=4–5). miR-150 expression is quantified taking U6 as an internal control while GAPDH was used as an internal control for quantifying pri-miR-150 expression. All bar graphs shows mean ± SEM. n is the number of mice/group. One way ANOVA and post-hoc t-test were used to compare data between groups (A and C–D). *P<0.05. In B, mice survival in from sepsis was assessed using log-rank test.