Fig. 2: Determination of whether loop3-deficient sclerostin by genetic truncation could maintain the protective effect of sclerostin on the cardiovascular system in ApoE−/− mice with loop3-deficient human sclerostin knock-in (Δloop3-SOSTki.ApoE−/−).
Comparisons were performed among wide-type mice with saline infusion (WT + saline), ApoE−/− mice with saline infusion (ApoE−/−+saline), ApoE−/− mice with AngII infusion (ApoE−/−+AngII), ApoE−/− mice with full-length human sclerostin knock-in and AngII infusion (hSOSTki. ApoE−/−+AngII) and ApoE−/− mice with loop3-deficient human sclerostin (1-110) knock-in and AngII infusion (Δloop3-SOSTki.ApoE−/−+AngII). a The incidence of AA formation. A two-sided chi-square test was performed to determine the difference between two groups. ****p < 0.0001. p < 0.0001 for all comparisons. b Ex vivo measurement of the maximum diameters of the aortic arches (left) and suprarenal aortas (right). Aortic arch: p < 0.0001 for all groups; suprarenal aortas: p < 0.0001 for all groups. c Quantification of positive Oil Red O staining per cryosection indicating the ratio of atherosclerotic plaque area to total cross cryosection area (%) of the aortic roots. p < 0.0001 for all groups. d Serum levels of inflammatory cytokines (IL-6, TNF-α) and chemokines (MCP-1). IL-6: p < 0.0001 for all groups; TNF- α: p < 0.0001 for all groups; MCP-1: p < 0.0001 for all groups. For (b to e), data were expressed as the mean ± standard deviation. n = 9 per group. One-way ANOVA with Tukey’s post-hoc test vs. ApoE−/−+AngII was used to determine the intergroup differences. ****p < 0.0001. Note: AA: aortic aneurysm; AngII: angiotensin II; IL-6: interleukin 6; MCP-1: monocyte chemoattractant protein-1; TNF-α: tumour necrosis factor alpha. Source data are provided as a Source Data file.
