Fig. 6: Determination of whether targeting sclerostin loop3 by the specific in vivo pharmacologic tool Apc001PE influenced the protective effect of overexpressed human sclerostin on the cardiovascular system by evaluating cardiovascular events in hSOSTki.ApoE−/− mice with AngII infusion. | Nature Communications

Fig. 6: Determination of whether targeting sclerostin loop3 by the specific in vivo pharmacologic tool Apc001PE influenced the protective effect of overexpressed human sclerostin on the cardiovascular system by evaluating cardiovascular events in hSOSTki.ApoE−/− mice with AngII infusion.

From: Targeting loop3 of sclerostin preserves its cardiovascular protective action and promotes bone formation

Fig. 6: Determination of whether targeting sclerostin loop3 by the specific in vivo pharmacologic tool Apc001PE influenced the protective effect of overexpressed human sclerostin on the cardiovascular system by evaluating cardiovascular events in hSOSTki.ApoE−/− mice with AngII infusion.

ApoE−/− mice or hSOSTki. ApoE−/− mice with AngII infusion were subcutaneously administered vehicle, Apc001PE (12 mg/kg) or humanized therapeutic sclerostin antibody (25 mg/kg) twice weekly for four weeks. After administration, the aortas were harvested for analysis. a The incidence of AA formation. A two-sided chi-square test was performed to determine the difference between groups. ****p < 0.0001. p < 0.0001 for all comparisons. b Ex vivo measurement of the maximum diameters of the aortic arches (left), thoracic aortas (middle) and suprarenal aortas (right). Aortic arch: p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody); thoracic aorta:, p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody); suprarenal aorta: p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody). c Quantification of positive staining per cryo-section of aortic roots stained with Oil Red O. p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody). d Serum levels of inflammatory cytokines (IL-6, TNF-α) and chemokines (MCP-1). IL = 6: p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody, p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody); TNF-α: p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody); MCP-1: p < 0.0001 (ApoE−/−-AngII+veh), p < 0.0001 (ApoE−/−-AngII+antibody), p < 0.0001 (hSOSTki. ApoE−/−-AngII+antibody). For (b to d), data were expressed as the mean ± standard deviation. n = 9 per group. ****p < 0.0001 for a comparison vs. hSOSTki. ApoE−/−-AngII+veh by one-way ANOVA with Tukey’s post-hoc test. Note: 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.

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