Skip to main content
Fig. 1 | BMC Biology

Fig. 1

From: In vivo genome and base editing of a human PCSK9 knock-in hypercholesterolemic mouse model

Fig. 1

Generation and characterization of the human PCSK9 knock-in mouse model (hPCSK9-KI). a Generation of the hPCSK9-KI mouse. A human PCSK9-cDNA expression cassette was inserted into the mouse Rosa26 locus. Red triangles indicate loxP sites flanking the Cre-Neo cassette in the targeting vector. The Neo gene was used for selection of positive clones, and the Diphtheria toxin A fragment gene (DTA) was used for negative selection of clones with random integrations of the transgene. Arrows indicate the genotyping primers; NdeI indicates the restriction enzyme site used for the neomycin probe (star) in Southern blot analysis. b, c Human PCSK9 and mouse Pcsk9 mRNA expression levels relative to β-actin in the liver from 10-week-old hPCSK9-KI mice and WT littermates (n = 4 per group). d Body weight in 28-week-old WT mice (n = 7) and hPCSK9-KI mice (n = 29). e, f Plasma concentrations of total cholesterol (CHO) and LDL cholesterol (LDL-C) in hPCSK9-KI mice and WT littermates at 10 and 28 weeks of age (n = 4 at 10 weeks; n = 7 for the WT group and n = 29 for the hPCSK9-KI group at 28 weeks). g Plasma concentrations of total cholesterol (CHO) 24 h after treatment with 10 mg/kg evolocumab in 13-week-old hPCSK9-KI mice and their WT littermates (n = 6 for the WT group and n = 8 for the hPCSK9-KI group). Student’s t test analysis was performed to evaluate the differences between WT and hPCSK9-KI mice. Values are presented as group means ± SEM. WT, wild type C57BL/6N. hPCSK9-KI, human PCSK9 inserted into Rosa26 locus in C57BL/6N. **p < 0.001, ***p < 0.0001, and ****p < 0.00001

Back to article page