Fig. 6: PDI deficiency impairs the assembly and secretion of ApoB-100 VLDL but not ApoB-48 VLDL.
a Twelve-week-old Pdifl/fl (n = 5) and Alb-cre/Pdifl/fl (n = 5) male mice were fasted for 16 h, followed by i.v. injection with tyloxapol at a concentration of 500 mg/kg body weight. Blood was collected before injection and after injection at 2 and 4 h. The levels of plasma TG were detected and the secretion rates of TG within 2 h were calculated. b The pooled mouse plasma of the same genotype was fractionated by size exclusion chromatography, TGs in different fractions were measured by commercial kits according to the manufacturer’s protocol. Different species of lipoproteins were indicated by arrows: VLDL (very-low-density lipoprotein), LDL (low-density lipoprotein), and HDL (high-density lipoprotein). c After size exclusion fractionation of plasma, the expressions of ApoB in every other fraction were examined by Western blotting. The blots of plasma from Pdifl/fl and Alb-cre/Pdifl/fl mice were set as control for normalization. d–i Fatty acid composition of VLDL isolated from Pdifl/fl and Alb-cre/Pdifl/fl mice (d), and from Dex and TM-treated mice (e) were ethylated and quantified using UHPLC-MS/MS. Total content of SFA and UFA in the VLDL were calculated by summing each of the SFA and UFA (f, g), and the proportion of SFA and UFA esters in these two types of VLDL were shown (h, i). n = 3 biological replicates in each group. Two-tailed Student’s t test were used. Data are presented as mean ± SEM. Source data are provided as a Source Data file.
