Skip to main content
. 2022 Mar 9;8(10):eabj2917. doi: 10.1126/sciadv.abj2917

Fig. 4. Hepatocyte KLF15 controls plasma corticosteroid bioavailability and inflammatory homeostasis via regulation of CBG in vivo.

Fig. 4.

(A) qRT-PCR analysis of Klf15 and Serpina6 mRNA expression in WT mouse primary hepatocytes stimulated with LPS (200 ng/ml). N = 3. *P < 0.05, **P < 0.02, and ***P < 0.01 by one-way ANOVA test followed by Bonferroni’s multiple comparison correction. (B) Survival of mice after intraperitoneal injection of LPS (15 μg/g of body weight LPS; N = 15). *P < 0.05 by log-rank test. (C) Plasma cytokine concentration in KLF15-LKO and control mice 24 hours after injection with LPS (12 μg/g of body weight) or saline. ***P < 0.01 for the effect of KLF15-LKO genotype status on LPS response using two-way ANOVA followed by Tukey’s multiple comparison test. A full panel of measured cytokines is provided in table S1. (D) Free and total corticosterone concentration in plasma of adult mice of the indicated genotypes (quantified by radioimmunoassay), measured 6 weeks after tail vein injection with indicated AAV8. N = 8 to 9. *P < 0.05 and ***P < 0.01 by two-way ANOVA followed by Tukey’s multiple comparison test. (E) Mice of indicated genotypes were given AAV8-CBG or AAV8-EV via tail vein injection. Six weeks after administration of AAV8, mice were given LPS (15 μg/g of body weight, intraperitoneally) and assessed for survival (N = 11 to 15). **P < 0.02 versus LKO + AAV8-EV by log-rank test. Data are shown as means ± SEM.