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. 2022 Nov 4;13:6647. doi: 10.1038/s41467-022-34433-z

Fig. 2. Oasl1 deficiency increases endothelial dysfunction, leading to vascular inflammation and leukocyte infiltration into the lesion.

Fig. 2

Apoe−/− and Oasl1−/−Apoe−/− mice were fed a normal chow diet (NCD) for 28 weeks to allow atherosclerotic conditions to develop. a Left: Oil red O-stained lesions in whole aortas. Right: Quantitation of stained areas in en face preparations (Total: p = 0.0040, R1: p = 0.0071, R2: p = 0.1175, R3: p = 0.0484, n = 9 per group). Yellow arrowhead: plaque in aorta. b–d Analysis of the transcriptomes of single cells from atherosclerotic aortas using the 10x Genomics platform. b Uniform manifold approximation and projection (UMAP) plot of 20,876 total aortic cells, colored by clusters. c Bar graphs showing the relative proportion of each cell type per group. d Dot plot showing Gene Set Enrichment Analysis (GSEA) according to the normalized enrichment score (NES) for Gene Ontology (GO) terms of aortas from Oasl1−/−Apoe−/− versus Apoe−/− mice. e Quantitative PCR analysis of the adhesion-related molecules in atherosclerotic aortas (Vcam1, Pecam1, F11r: p = 0.4857, Icam1, Selplg, Sele: p = 0.0286, Icam2: p = 0.2000, n = 4 per group). f, g Flow cytometry of single cells obtained from atherosclerotic aortas (n = 8 per group), including total leukocytes (f) and macrophages (p = 0.0499), neutrophils (p = 0.0433), and dendritic cells (DC; p = 0.1755) (g). Data in a are representative of each group. a, f and g, Box plots are shown as median of each value and the interquartile range (IQR, the range between the 25th and 75th percentiles); whiskers indicate 1.5 times the IQR. Data are presented as the means ± SEMs (*p ≤ 0.05, **p ≤ 0.01; a, f and g, two-sided unpaired Student’s t-test; e, two-sided Mann-Whitney U test). Source data are provided as a Source Data file.