Figure 2. Decreased contractile smooth muscle cell (SMC) population and contractile gene expression and increased pro-inflammatory SMC population and inflammatory gene expression in the aorta of angiotensin II (AngII)-infused mice.

A, Uniform manifold approximation and projection (UMAP) plots representing the intercluster similarity in the aorta among control, non-dissection, and dissection aortas with GFP+ and RFP+ cells separately. B, A bar plot representing the percentage of different SMC subclusters in the GFP+ cells from aortas of control, non-dissection, and dissection mice. The chi-square test of goodness-of-fit was performed to compare the proportion between groups; the p values were adjusted by Bonferroni correction. C-D, RNA velocity analysis was performed to estimate the transition of aortic SMCs induced by aortic challenge. E, Heatmap showing the row-scaled mean expression of DEGs identified from non-dissection vs control, and from dissection vs non-dissection. DEGs were classified according to their expression profiles across 3 samples. F, The top biological process enriched from decreased DEGs (green bars) and increased DEGs (red bars) in GFP+ SMCs of AngII-infused mice. G, Heatmap showing the mean expression of contractile and inflammatory genes expression in GFP+ SMCs in control, non-dissection, and dissection samples. H, Violin plot showing the distribution of Myh11, Myl9, and Cxcl12 expression values in GFP+ SMCs of control, non-dissection, and dissection samples. Black dots in the violins indicate the median values. The Wilcoxon rank sum test was performed to compare the genes between two groups; p values were adjusted by Bonferroni correction using all genes in the dataset. I, Immunofluorescence analysis of mT/mG lineage tracing showing SM22α and IL-1β expression in the aortic tissue of WT mice infused with saline (left panel) or AngII (right panel).