Extended Data Fig. 2: Upregulation of SEMA3A in primary human LSEC by palmitic acid and forskolin.
From: Semaphorin-3A regulates liver sinusoidal endothelial cell porosity and promotes hepatic steatosis
a, SEMA3A mRNA expression in primary human LSEC (female donor; QC-29B15F09) treated for 24 h with 0.5 mM palmitic acid (n = 2 independent experiments, left n = 3, and right n = 6 wells per condition). b, Graphical overview of transcription factor (TF) binding sites predicted by CiiiDER (upper panel) and selected binding sites for CREB1, PPARs, and SREBFs (lower panel). c, SEMA3A mRNA expression in primary human LSEC (male donor; QC-12B15F11) treated with 100 µM forskolin (FSK) for 2, 4, and 6 h compared to DMSO-treated cells (n = 3 independent experiments). d, SEMA3A mRNA expression in HepG2 cells and primary human LSEC (male donor QC-12B15F11) after treatment with 100 µM FSK or DMSO for 6 h (n = 3 independent experiments). A two-tailed unequal variances t-test was used to test for statistical significance in (a). A one-way ANOVA with Dunnett´s post hoc test (c) and two-way ANOVA with Tukey´s post hoc test (d) were also used to test for statistical significance. In all graphs individual data points and mean ± SEM are presented.
