Fig 1: Proteomic analyses reveal activation of AngII signaling pathways in SMAs of smLRP1–/– mice.(A) Principal component analysis of the LRP1+/+ (n = 5) versus smLRP1–/– (KO) (n = 4) samples from 14-week-old mice. (B) Volcano plot showing –log10 FDR (y axis) versus log2 fold-change (FC) for each protein (orange, FDR < 0.01, FC > |2|; gray, FDR > 0.01). (C) Intensity levels for LRP1 in LRP1+/+ and smLRP1–/– mice. (D) Gene ontology enrichment analysis for upregulated (left panel) or downregulated (right panel) pathways. (E) Log2 fold-change for selected LRP1 ligands as determined by mass spectral intensities. (F) Activation z scores for selected pathways and (G) P values of overlap for pathways identified in IPA software. (H) Fold-changes in myocardin-regulated proteins in smLRP1–/– mice relative to LRP1+/+ as quantified by mass spectrometry.
Fig 2: AGT ASO administration restores the arterial phenotype of smLRP1–/– mice.Six-week-old mice were injected subcutaneously with AGT ASO on days 1 and 4 and then weekly for 11 weeks. At 18 weeks of age, mice were sacrificed. (A) Plasma AGT concentrations were quantified by ELISA; (B) lumen diameters of SMAs were quantified by ultrasonography; and (C) ex vivo widths of SMAs from LRP1+/+ and smLRP1–/– mice were measured (2-way ANOVA, Tukey’s multiple-comparison test).
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