Figure 3

In mice, treatment with angiotensin II (Ang II) and β-aminopropionitrile (BAPN) causes acute inflammation before aortic dissection occurs. (A) Gross morphology of aortic dissection (AD) in male C57BL/6J mice; aortas in control mice without Ang II or BAPN treatment (Control), aortas without AD after exposure to ANGII (1 µg/kg/µl) and BAPN (5 g/drinking water) (No-AD), and aortas with AD after exposure to ANGII and BAPN (AD). (B,C) Flow cytometric analysis showing percentages with plots after gating of CD45⁺ immune cells excluding doublets (B) and cell numbers of total CD45⁺ cells, neutrophils, Ly6C^high monocytes, and macrophages (C). (n = 5 controls, n = 4 Non-AD, n = 5 AD). One-way analysis of variance with Tukey’s multiple comparison test; *P < 0.05. (D) Uniform manifold approximation and projection (UMAP) dimensionality reduction analysis identifying unique immune populations in male mice exposed to Ang II (1 µg/kg/µl) and BAPN (5 g/l in drinking water) for 1 week. (E) Dot plots displaying the signature cell gene expression markers. (F,G) CellChat showing the activated interaction between each cell population in the interleukin-1 (IL-1) signaling pathway. (H) Feature plots of IL-1β and Il1r1 expression on UMAP. CellChat; a tool that can quantitatively infer and analyze intercellular communication networks from scRNA-seq data. Macs macrophages, Monos monocytes, DCs dendritic cells, NK cells natural killer cells, ILCs Innate lymphoid cells, VSMCs vascular smooth muscle cells, ECs endothelial cells.