Fig. 2: LSECs are a major source of CXCL chemokines in the liver under the control of TNFα/NF-κB signaling.
From: Super enhancer regulation of cytokine-induced chemokine production in alcoholic hepatitis
a RNA-seq of normal liver cell types. Expression levels of CXCL genes (expressed in RPKM) were normalized (see supplemental methods for normalization details) and ratios are plotted. Data represented as mean ± SD. One-way ANOVA analysis was performed, with post hoc Dunnett’s multiple comparison correction (n = 3 biologically independent samples for each cell type). b TNFα significantly increased expression of CXCL chemokines revealed by qPCR (n = 4, biologically independent samples from two independent experiments, experiments repeated more than five times with similar results) and by ELISA (n = 11, biologically independent samples from three independent experiments). CXCL chemokines expression is shown as fold change over control condition for qPCR and as pg/ml by ELISA. Data represented as mean ± SD. A two-sided, paired t-test analysis was performed. c LSECs were pretreated with varying amounts of Celastrol (0 to 5 μM) and exposed to medium with or without TNFα. qPCRs were performed for quantifying the expression of CXCL1, 6, and 8, and shown in log10 fold over basal expression. Data represented as mean ± SD. One-way matched-pairs ANOVA analysis was performed with post hoc Dunnett’s multiple comparison correction (n = 6, biologically independent samples from three independent experiments). There was a significant linear trend of decreasing CXCL1, 6, 8 expressions with increasing Celastrol concentrations with TNFα (p < 0.0001 for all groups).
