Fig. 2: SEMA3A expression is upregulated in human LSECs after treatment with palmitic acid.
From: Semaphorin-3A regulates liver sinusoidal endothelial cell porosity and promotes hepatic steatosis
a,b, SEMA3A-G mRNA expression in primary human LSECs (male donor QC-12B15F11) treated for 18 h with BSA control (n = 4 wells) versus 0.75 mM palmitic acid (n = 5 wells) (a) or oleic acid versus BSA controls (n = 6 wells each) (b). c–f, Expression of SEMA3A in primary human LSECs after treatment with BSA control (n = 4 palmitic acid-, n = 6 oleic acid-treated wells) versus 0.25 mM (n = 5, n = 6 wells), 0.5 mM (n = 4, n = 6 wells) and 0.75 mM (n = 5, n = 6 wells) BSA-bound palmitic acid (c) or oleic acid (e). Expression of SEMA3A in primary human LSECs treated with BSA controls (n = 4 wells each), 0.5 mM palmitic acid (d) or oleic acid (f) for 2 h (n = 5 wells each), 6 h (n = 6, n = 5 wells), 18 h (n = 4, n = 5 wells) and 24 h (n = 5 wells each). A multiple two-tailed unpaired t-test with a two-stage step-up method was used to discover outstanding effects84, as indicated by q values in a,b. A one-way ANOVA with Dunnett’s post hoc test was used to test for statistical significance in c–f. In all graphs individual data points and mean ± s.e.m. are presented.
